Journal articles: 'MYB42'

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Geng, Pan, Su Zhang, Jinyue Liu, Cuihuan Zhao, Jie Wu, Yingping Cao, Chunxiang Fu, Xue Han, Hang He, and Qiao Zhao. "MYB20, MYB42, MYB43, and MYB85 Regulate Phenylalanine and Lignin Biosynthesis during Secondary Cell Wall Formation." Plant Physiology 182, no. 3 (December 23, 2019): 1272–83. http://dx.doi.org/10.1104/pp.19.01070.

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Zhang, Zuying, Changtao Li, Hui Zhang, Yeqing Ying, Yuanyuan Hu, and Lili Song. "Comparative Analysis of the Lignification Process of Two Bamboo Shoots Stored at Room Temperature." Plants 9, no. 10 (October 21, 2020): 1399. http://dx.doi.org/10.3390/plants9101399.

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Two types of bamboo shoots, high bamboo (Phyllostachys prominens) shoots (HBSes) and moso bamboo (Phyllostachys edulis) shoots (MBSes), underwent a fast post-harvest lignification process under room temperature storage. To explore the mechanism of lignification in two types of bamboo shoots after post-harvest during room temperature storage, the measurement of cell wall polymers (lignin and cellulose) and enzyme activities of phenylalanine ammonialyase (PAL) and peroxidase (POD), and relative expression of related transcription networks factors (TFs) were performed. The results suggested that the lignification process in HBSes is faster than that in MBSes because of incremental increase in lignin and cellulose contents within 6 days and the shorter shelf-life. Additionally, compared with the expression pattern of lignification-related TFs and correlation analysis of lignin and cellulose contents, MYB20, MYB43, MYB85 could function positively in the lignification process of two types of bamboo shoots. A negative regulator, KNAT7, could negatively regulate the lignin biosynthesis in two types of bamboo shoots. In addition, MYB63 could function positively in HBSes, and NST1 could function negatively in MBSes. Notably, MYB42 may function differently in the two types of bamboo shoots, that is, a positive regulator in HBSes, but a negative regulator in MBSes. Transcription networks provide a comprehensive analysis to explore the mechanism of lignification in two types of bamboo shoots after post-harvest during room temperature storage. These results suggest that the lignification of bamboo shoots was mainly due to the increased activity of POD, higher expression levels of MYB20, MYB43, MYB63, and MYB85 genes, and lower expression levels of KNAT7 and NST1 genes, and the lignification process of HBSes and MBSes had significant differences.

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Sun, Yuhui, Jun Zhao, Xinyue Li, and Yingzhang Li. "E2 conjugases UBC1 and UBC2 regulate MYB42‐mediated SOS pathway in response to salt stress in Arabidopsis." New Phytologist 227, no. 2 (April 19, 2020): 455–72. http://dx.doi.org/10.1111/nph.16538.

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Wang, Nan, Haifeng Xu, Shenghui Jiang, Zongying Zhang, Ninglin Lu, Huarong Qiu, Changzhi Qu, Yicheng Wang, Shujing Wu, and Xuesen Chen. "MYB12 and MYB22 play essential roles in proanthocyanidin and flavonol synthesis in red-fleshed apple (Malus sieversiif. niedzwetzkyana)." Plant Journal 90, no. 2 (February 27, 2017): 276–92. http://dx.doi.org/10.1111/tpj.13487.

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Qi, Xin, Wensi Tang, Weiwei Li, Zhang He, Weiya Xu, Zhijin Fan, Yongbin Zhou, et al. "Arabidopsis G-Protein β Subunit AGB1 Negatively Regulates DNA Binding of MYB62, a Suppressor in the Gibberellin Pathway." International Journal of Molecular Sciences 22, no. 15 (July 31, 2021): 8270. http://dx.doi.org/10.3390/ijms22158270.

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Plant G proteins are versatile components of transmembrane signaling transduction pathways. The deficient mutant of heterotrimeric G protein leads to defects in plant growth and development, suggesting that it regulates the GA pathway in Arabidopsis. However, the molecular mechanism of G protein regulation of the GA pathway is not understood in plants. In this study, two G protein β subunit (AGB1) mutants, agb1-2 and N692967, were dwarfed after exogenous application of GA3. AGB1 interacts with the DNA-binding domain MYB62, a GA pathway suppressor. Transgenic plants were obtained through overexpression of MYB62 in two backgrounds including the wild-type (MYB62/WT Col-0) and agb1 mutants (MYB62/agb1) in Arabidopsis. Genetic analysis showed that under GA3 treatment, the height of the transgenic plants MYB62/WT and MYB62/agb1 was lower than that of WT. The height of MYB62/agb1 plants was closer to MYB62/WT plants and higher than that of mutants agb1-2 and N692967, suggesting that MYB62 is downstream of AGB1 in the GA pathway. qRT-PCR and competitive DNA binding assays indicated that MYB62 can bind MYB elements in the promoter of GA2ox7, a GA degradation gene, to activate GA2ox7 transcription. AGB1 affected binding of MYB62 on the promoter of GA2ox7, thereby negatively regulating th eactivity of MYB62.

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Im, Jong Hee, Jae-Heung Ko, Won-Chan Kim, Brent Crain, Daniel Keathley, and Kyung-Hwan Han. "Mitogen-activated protein kinase 6 negatively regulates secondary wall biosynthesis by modulating MYB46 protein stability in Arabidopsis thaliana." PLOS Genetics 17, no. 4 (April 7, 2021): e1009510. http://dx.doi.org/10.1371/journal.pgen.1009510.

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The R2R3-MYB transcription factor MYB46 functions as a master switch for secondary cell wall biosynthesis, ensuring the exquisite expression of the secondary wall biosynthetic genes in the tissues where secondary walls are critical for growth and development. At the same time, suppression of its function is needed when/where formation of secondary walls is not desirable. Little is known about how this opposing control of secondary cell wall formation is achieved. We used both transient and transgenic expression of MYB46 and mitogen-activated protein kinase 6 (MPK6) to investigate the molecular mechanism of the post-translational regulation of MYB46. We show that MYB46 is phosphorylated by MPK6, leading to site specific phosphorylation-dependent degradation of MYB46 by the ubiquitin-mediated proteasome pathway. In addition, the MPK6-mediated MYB46 phosphorylation was found to regulate in planta secondary wall forming function of MYB46. Furthermore, we provide experimental evidences that MYB83, a paralog of MYB46, is not regulated by MPK6. The coupling of MPK signaling to MYB46 function provides insights into the tissue- and/or condition-specific activity of MYB46 for secondary wall biosynthesis.

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Chen, Jianli, and Xiaowen Chen. "MYBL2 Is Targeted by miR-143-3p and Regulates Breast Cancer Cell Proliferation and Apoptosis." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 26, no. 6 (July 5, 2018): 913–22. http://dx.doi.org/10.3727/096504017x15135941182107.

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Breast cancer remains a public health issue on a global scale. The present study aimed to explore the functional role of MYB proto-oncogene like 2 (MYBL2) in breast cancer, as well as underlying mechanisms. The regulatory relationship between miR-143-3p and MYBL2 was analyzed, and the effects of dysregulation of miR-143-3p and MYBL2 on cell proliferation and apoptosis were investigated. The results showed that MYBL2 and miR-143-3p were inversely expressed in breast cancer tissues and cells: MYBL2 was highly expressed, whereas miR-143-3p was lowly expressed. MYBL2 was confirmed as a target gene of miR-143-3p. Suppression of MYBL2 inhibited proliferation and induced apoptosis of breast cancer cells, which was similar to the effects of overexpression of miR-143-3p. Our findings reveal that MYBL2 is targeted by miR-143-3p and regulates breast cancer cell proliferation and apoptosis.

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Yoshikawa, Yuki, Xin Victoria Wang, Yu-Hui Chen, Ying Zhang Mazzu, Goutam Chakraborty, Lina E. Jehane, Sai Harisha Rajanala, et al. "The impact of the expression of the transcription factor MYBL2 on outcomes of patients with localized and advanced prostate cancer." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 149. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.149.

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149 Background: Patients with metastatic hormone-sensitive prostate cancer (mHSPC) have a variable response to ADT and some benefit from the addition of docetaxel or an androgen signaling pathway inhibitor. We found that loss of the epigenetic regulator KDM5D is associated with more aggressive prostate cancer (PC). We sought to determine whether MYBL2 which is regulated by KDM5D mediates this effect. MYBL2 is a transcription factor which controls key genes (e.g. FOXM1) and increases cell cycle progression and survival. Methods: AR expressing hormone-sensitive cell lines, LNCaP and LAPC4 were used. Motif analysis and CHiPseq of LNCaP with and without siKDM5D was performed and impact of modulation of KDM5D and MYBL2 in both cells on cell survival was assessed. Gene expression profiling (GEP) data assessed MYBL2’s association with KDM5D levels in localized disease (publicly available data) and mHSPC (Decipher whole Affymetrix platform on CHAARTED samples). Results: Silencing KDM5D increased H3K4me3 and increased MYBL2 expression. GEP showed a strong negative correlation between KDM5D and MYBL2 in patients with localized PC (-0.66; TCGA) but not from primary prostate cancer tissue with mHSPC (-0.03; CHAARTED). Cells with low KDM5D and high MYBL2 were androgen independent and more resistant to docetaxel. In TCGA, patients with high MYBL2 had a higher rate of relapse from localized disease. In patients with metastatic disease (CHAARTED) low MYBL2 was associated with a better overall survival (OS) on multivariable analysis when treated with ADT or ADT + docetaxel. Conclusions: Low MYBL2 is associated with a longer OS with ADT alone and ADT and docetaxel independent of clinical variables. Patients with high MYBL2 expression had better OS with ADT plus docetaxel compared with patients with high MYBL2 treated with ADT alone.[Table: see text]

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Zhang, Xueying, Yuqing He, Linying Li, Hongru Liu, and Gaojie Hong. "Involvement of the R2R3-MYB transcription factor MYB21 and its homologs in regulating flavonol accumulation in Arabidopsis stamen." Journal of Experimental Botany 72, no. 12 (April 8, 2021): 4319–32. http://dx.doi.org/10.1093/jxb/erab156.

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Abstract Commonly found flavonols in plants are synthesized from dihydroflavonols by flavonol synthase (FLS). The genome of Arabidopsis thaliana contains six FLS genes, among which FLS1 encodes a functional enzyme. Previous work has demonstrated that the R2R3-MYB subgroup 7 transcription factors MYB11, MYB12, and MYB111 redundantly regulate flavonol biosynthesis. However, flavonol accumulation in pollen grains was unaffected in the myb11myb12myb111 triple mutant. Here we show that MYB21 and its homologs MYB24 and MYB57, which belong to subgroup 19, promote flavonol biosynthesis through regulation of FLS1 gene expression. We used a combination of genetic and metabolite analysis to identify the role of MYB21 in regulating flavonol biosynthesis through direct binding to the GARE cis-element in the FLS1 promoter. Treatment with kaempferol or overexpression of FLS1 rescued stamen defects in the myb21 mutant. We also observed that excess reactive oxygen species (ROS) accumulated in the myb21 stamen, and that treatment with the ROS inhibitor diphenyleneiodonium chloride partly rescued the reduced fertility of the myb21 mutant. Furthermore, drought increased ROS abundance and impaired fertility in myb21, myb21myb24myb57, and chs, but not in the wild type or myb11myb12myb111, suggesting that pollen-specific flavonol accumulation contributes to drought-induced male fertility by ROS scavenging in Arabidopsis.

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Shukla, Vinay, Jian-Pu Han, Fabienne Cléard, Linnka Lefebvre-Legendre, Kay Gully, Paulina Flis, Alice Berhin, et al. "Suberin plasticity to developmental and exogenous cues is regulated by a set of MYB transcription factors." Proceedings of the National Academy of Sciences 118, no. 39 (September 22, 2021): e2101730118. http://dx.doi.org/10.1073/pnas.2101730118.

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Suberin is a hydrophobic biopolymer that can be deposited at the periphery of cells, forming protective barriers against biotic and abiotic stress. In roots, suberin forms lamellae at the periphery of endodermal cells where it plays crucial roles in the control of water and mineral transport. Suberin formation is highly regulated by developmental and environmental cues. However, the mechanisms controlling its spatiotemporal regulation are poorly understood. Here, we show that endodermal suberin is regulated independently by developmental and exogenous signals to fine-tune suberin deposition in roots. We found a set of four MYB transcription factors (MYB41, MYB53, MYB92, and MYB93), each of which is individually regulated by these two signals and is sufficient to promote endodermal suberin. Mutation of these four transcription factors simultaneously through genome editing leads to a dramatic reduction in suberin formation in response to both developmental and environmental signals. Most suberin mutants analyzed at physiological levels are also affected in another endodermal barrier made of lignin (Casparian strips) through a compensatory mechanism. Through the functional analysis of these four MYBs, we generated plants allowing unbiased investigation of endodermal suberin function, without accounting for confounding effects due to Casparian strip defects, and were able to unravel specific roles of suberin in nutrient homeostasis.

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Liang, Hai-Bin, Yang Cao, Qiang Ma, Yi-Jun Shu, Zheng Wang, Fei Zhang, Yuan-Yuan Ye, et al. "MYBL2 is a Potential Prognostic Marker that Promotes Cell Proliferation in Gallbladder Cancer." Cellular Physiology and Biochemistry 41, no. 5 (2017): 2117–31. http://dx.doi.org/10.1159/000475454.

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Background: Gallbladder cancer (GBC) is an aggressive and highly lethal biliary tract malignancy, with extremely poor prognosis. In the present study, we analyzed the potential involvement of MYBL2, a member of the Myb transcription factor family, in the carcinogenesis of human GBC. Methods: MYBL2 expression levels were measured in GBC and cholecystitis tissue specimens using quantitative real-time PCR (qRT-PCR) and immunohistochemical (IHC) assays. The effects of MYBL2 on cell proliferation and DNA synthesis were evaluated using Cell Counting Kit-8 assay (CCK-8), colony formation, and 5-ethynyl-2'-deoxyuridine (EdU) retention assay, flow cytometry analysis, western blot, and a xenograft model of GBC cells in nude mice. Results: MYBL2 expression was increased in GBC tissues and associated with histological differentiation, tumour invasion, clinical stage and unfavourable overall survival in GBC patients. The downregulation of MYBL2 expression resulted in the inhibition of GBC cell proliferation, and DNA replication in vitro, and the growth of xenografted tumours in nude mice. Conversely, MYBL2 overexpression resulted in the opposite effects. Conclusions: MYBL2 overexpression promotes GBC cell proliferation through the regulation of the cell cycle at the S and G2/M phase transitions. Thus, MYBL2 could serve as a potential prognostic and therapeutic biomarker in GBC patients.

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Heinrichs, Stefan, Lily Conover, Carlos E. Bueso-Ramos, Outi Kilpivaara, Ross Levine, Kristen Stevenson, Donna Neuberg, et al. "MYBL2 Is a Candidate Tumor Suppressor Gene In MDS." Blood 116, no. 21 (November 19, 2010): 1865. http://dx.doi.org/10.1182/blood.v116.21.1865.1865.

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Abstract Abstract 1865 Cytogenetic changes, mainly deletions, can be found in about 30–50% of patients with Myelodysplastic Syndromes (MDS). To identify a tumor suppressor candidate within a commonly deleted region on chromosome 20q, we performed gene expression analysis on CD34+ bone marrow cells obtained from 8 patients with a 20q aberration and 18 with a normal karyotype. However, we were unable to identify genes that were significantly differentially expressed in aberrant 20q karyotype as compared to normal karyotype MDS patients. In contrast, a comparison of CD34+ cells from all MDS cases analyzed (n=26) with CD34+ cells obtained from normal bone marrow (n=4) revealed 108 genes that were differentially expressed. Interestingly, one of the top-scoring genes was MYBL2, which is located on chromosome 20q. MYBL2 levels were downregulated more than two-fold in 18 out of 26 cases. RNAi-mediated knockdown of MYBL2 in CD34+ normal bone marrow cells revealed a signature of genes functionally associated with the G2/M cell cycle phase confirming the well-documented role of MYBL2 as key transcription factor governing the onset of cell division. We hypothesize that in a subset of MDS cases the control of cell division may be impaired by low levels of MYBL2 such that altered cell fates established during cell division in early hematopoietic stem and progenitor cells will lead to clonal expansion with imbalanced or impaired differentiation. Indeed, gene set enrichment analysis revealed a strong enrichment of MYBL2 signature genes in MDS CD34+ cells. In support of a potential role as tumor suppressor, resequencing of MYBL2 (144 patients) identified 2 somatic mutations, pinpointing an additional mechanism to reduce expression of normal levels of wild-type MYBL2. Disclosures: No relevant conflicts of interest to declare.

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Morris, Benjamin B., Lisa G. Gray, Ryan D. Gentzler, David Randolph Jones, and Marty W. Mayo. "Omics guided small molecule inhibitor screen for the identification of therapeutic vulnerabilities in metastatic lung adenocarcinoma." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e21015-e21015. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e21015.

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e21015 Background: Recent studies from our lab and others have demonstrated that double-strand DNA break accumulation, error-prone repair, and genomic instability are strongly linked to increased metastasis to distant organs. Our lab has shown that lung adenocarcinomas overexpressing the transcription factor MYBL2 display chronic replication stress, elevated error-prone repair, and widespread genomic instability. Importantly, this MYBL2-driven phenotype accounts for ̃21% of all lung adenocarcinomas and identifies aggressive disease enriched for metastases to brain, liver, and kidney. This study was performed to identify clinically actionable therapeutic vulnerabilities in MYBL2-driven metastatic lung adenocarcinoma. Methods: RNA-sequencing and proteomic data from the TCGA and ORIEN consortiums were mined to identify highly expressed druggable targets in MYBL2-driven lung adenocarcinomas. Identified targets were used to assemble a custom inhibitor library of 50 small molecules targeting DNA repair effectors, epigenetic factors, protein translation, kinase-signaling, autophagy, and post-translational modifications. Omics data from the Cancer Cell Line Encyclopedia was used to identify human cell line models (H1650 (pleura), H1568 (lymph node), H1299 (lymph node)) of MYBL2-driven metastatic disease. Inhibitors were tested at two doses, 5 uM and 500 nM, in triplicate, across replicate experiments. The PrestoBlue HS viability reagent was used to quantify cell viability in a 96 well plate format. The primary endpoint of this study was statistically significant cancer cell death, compared to vehicle controls. Results: Screen results demonstrated that, at nanomolar doses, inhibitors of protein translation have strong anti-tumor effects in MYBL2-driven disease. Interestingly, small molecules targeting EIF4G1 (SBI-0640756), ribosome biogenesis/RNA export (YM155), and rRNA synthesis (CX5461) were effective in inducing cell death while inhibitors blocking mTOR signaling, EIF2A phosphorylation, and EIF4F complex assembly were not. Bioinformatic analysis revealed that ̃60% of MYBL2-driven transcripts are dependent on EIF4G1 for translation. Importantly, effected transcripts include effectors controlling DNA repair, cell cycle coordination, and cell survival. Conclusions: Our data demonstrates that MYBL2-driven metastatic disease is uniquely sensitive to inhibitors of the protein translation machinery. Importantly, these inhibitors significantly outperform current standard-of-care agents cisplatin and pemetrexed. To our knowledge, our study is the first to demonstrate that blocking EIF4G1 effectively induces widespread cell death in metastatic lung adenocarcinoma models. Collectively, our work supports initiation of clinical trials testing the efficacy of SBI-0640756 in MYBL2-driven metastatic lung adenocarcinoma.

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Stringlis, Ioannis A., Ke Yu, Kirstin Feussner, Ronnie de Jonge, Sietske Van Bentum, Marcel C. Van Verk, Roeland L. Berendsen, Peter A. H. M. Bakker, Ivo Feussner, and Corné M. J. Pieterse. "MYB72-dependent coumarin exudation shapes root microbiome assembly to promote plant health." Proceedings of the National Academy of Sciences 115, no. 22 (April 23, 2018): E5213—E5222. http://dx.doi.org/10.1073/pnas.1722335115.

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Plant roots nurture a tremendous diversity of microbes via exudation of photosynthetically fixed carbon sources. In turn, probiotic members of the root microbiome promote plant growth and protect the host plant against pathogens and pests. In the Arabidopsis thaliana–Pseudomonas simiae WCS417 model system the root-specific transcription factor MYB72 and the MYB72-controlled β-glucosidase BGLU42 emerged as important regulators of beneficial rhizobacteria-induced systemic resistance (ISR) and iron-uptake responses. MYB72 regulates the biosynthesis of iron-mobilizing fluorescent phenolic compounds, after which BGLU42 activity is required for their excretion into the rhizosphere. Metabolite fingerprinting revealed the antimicrobial coumarin scopoletin as a dominant metabolite that is produced in the roots and excreted into the rhizosphere in a MYB72- and BGLU42-dependent manner. Shotgun-metagenome sequencing of root-associated microbiota of Col-0, myb72, and the scopoletin biosynthesis mutant f6′h1 showed that scopoletin selectively impacts the assembly of the microbial community in the rhizosphere. We show that scopoletin selectively inhibits the soil-borne fungal pathogens Fusarium oxysporum and Verticillium dahliae, while the growth-promoting and ISR-inducing rhizobacteria P. simiae WCS417 and Pseudomonas capeferrum WCS358 are highly tolerant of the antimicrobial effect of scopoletin. Collectively, our results demonstrate a role for coumarins in microbiome assembly and point to a scenario in which plants and probiotic rhizobacteria join forces to trigger MYB72/BGLU42-dependent scopolin production and scopoletin excretion, resulting in improved niche establishment for the microbial partner and growth and immunity benefits for the host plant.

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Chen, Yi-Shih, Tuan-Hua David Ho, Lihong Liu, Ding Hua Lee, Chun-Hua Lee, Yi-Ru Chen, Shu-Yu Lin, Chung-An Lu, and Su-May Yu. "Sugar starvation-regulated MYBS2 and 14-3-3 protein interactions enhance plant growth, stress tolerance, and grain weight in rice." Proceedings of the National Academy of Sciences 116, no. 43 (October 8, 2019): 21925–35. http://dx.doi.org/10.1073/pnas.1904818116.

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Autotrophic plants have evolved distinctive mechanisms for maintaining a range of homeostatic states for sugars. The on/off switch of reversible gene expression by sugar starvation/provision represents one of the major mechanisms by which sugar levels are maintained, but the details remain unclear. α-Amylase (αAmy) is the key enzyme for hydrolyzing starch into sugars for plant growth, and it is induced by sugar starvation and repressed by sugar provision. αAmy can also be induced by various other stresses, but the physiological significance is unclear. Here, we reveal that the on/off switch of αAmy expression is regulated by 2 MYB transcription factors competing for the same promoter element. MYBS1 promotes αAmy expression under sugar starvation, whereas MYBS2 represses it. Sugar starvation promotes nuclear import of MYBS1 and nuclear export of MYBS2, whereas sugar provision has the opposite effects. Phosphorylation of MYBS2 at distinct serine residues plays important roles in regulating its sugar-dependent nucleocytoplasmic shuttling and maintenance in cytoplasm by 14-3-3 proteins. Moreover, dehydration, heat, and osmotic stress repress MYBS2 expression, thereby inducing αAmy3. Importantly, activation of αAmy3 and suppression of MYBS2 enhances plant growth, stress tolerance, and total grain weight per plant in rice. Our findings reveal insights into a unique regulatory mechanism for an on/off switch of reversible gene expression in maintaining sugar homeostatic states, which tightly regulates plant growth and development, and also highlight MYBS2 and αAmy3 as potential targets for crop improvement.

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Chu, Chien-Hsin, Lung-Chun Chang, Hong-Ming Hsu, Shu-Yi Wei, Hsing-Wei Liu, Yu Lee, Chung-Chi Kuo, et al. "A Highly Organized Structure Mediating Nuclear Localization of a Myb2 Transcription Factor in the Protozoan Parasite Trichomonas vaginalis." Eukaryotic Cell 10, no. 12 (October 21, 2011): 1607–17. http://dx.doi.org/10.1128/ec.05177-11.

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ABSTRACT Nuclear proteins usually contain specific peptide sequences, referred to as nuclear localization signals (NLSs), for nuclear import. These signals remain unexplored in the protozoan pathogen, Trichomonas vaginalis . The nuclear import of a Myb2 transcription factor was studied here using immunodetection of a hemagglutinin-tagged Myb2 overexpressed in the parasite. The tagged Myb2 was localized to the nucleus as punctate signals. With mutations of its polybasic sequences, 48KKQK51 and 61KR62, Myb2 was localized to the nucleus, but the signal was diffusive. When fused to a C-terminal non-nuclear protein, the Myb2 sequence spanning amino acid (aa) residues 48 to 143, which is embedded within the R2R3 DNA-binding domain (aa 40 to 156), was essential and sufficient for efficient nuclear import of a bacterial tetracycline repressor (TetR), and yet the transport efficiency was reduced with an additional fusion of a firefly luciferase to TetR, while classical NLSs from the simian virus 40 T-antigen had no function in this assay system. Myb2 nuclear import and DNA-binding activity were substantially perturbed with mutation of a conserved isoleucine (I74) in helix 2 to proline that altered secondary structure and ternary folding of the R2R3 domain. Disruption of DNA-binding activity alone by point mutation of a lysine residue, K51, preceding the structural domain had little effect on Myb2 nuclear localization, suggesting that nuclear translocation of Myb2, which requires an ordered structural domain, is independent of its DNA binding activity. These findings provide useful information for testing whether myriad Mybs in the parasite use a common module to regulate nuclear import.

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Hsu, Hong-Ming, Shiou-Jeng Ong, Ming-Chun Lee, and Jung-Hsiang Tai. "Transcriptional Regulation of an Iron-Inducible Gene by Differential and Alternate Promoter Entries of Multiple Myb Proteins in the Protozoan Parasite Trichomonas vaginalis." Eukaryotic Cell 8, no. 3 (January 16, 2009): 362–72. http://dx.doi.org/10.1128/ec.00317-08.

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ABSTRACT Iron-inducible transcription of a malic enzyme gene (also reputed to be ap65-1) in Trichomonas vaginalis was previously shown to involve a Myb1 repressor and a Myb2 activator, each of which may preferentially select two closely spaced promoter sites, MRE-1/MRE-2r, which comprises overlapping promoter elements, and MRE-2f. In the present study, an iron-inducible ∼32-kDa Myb3 nuclear protein was demonstrated to bind only the MRE-1 element. Changes in the iron supply, which produced antagonistic effects on the levels of Myb2 and Myb3 expression, also resulted in temporal and alternate entries of Myb2 and Myb3 into the ap65-1 promoter. Repression or activation of basal and iron-inducible ap65-1 transcription was detected in transfected cells when Myb3 was, respectively, substantially knocked down or overexpressed. In the latter case, increased Myb3 promoter entry was detected with concomitant decrease in Myb2 promoter entry under specific conditions, while Myb3 promoter entry was inhibited under all test conditions in cells overexpressing Myb2. In contrast, concomitant promoter entries by Myb2 and Myb3 diminished in cells overexpressing Myb1, except that Myb3 promoter entry was slightly affected under prolonged iron depletion. Together, these results suggest that Myb2 and Myb3 may coactivate basal and iron-inducible ap65-1 transcription against Myb1 through conditional and competitive promoter entries.

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Papetti, Michael, and Leonard H. Augenlicht. "Mybl2, downregulated during colon epithelial cell maturation, is suppressed by miR-365." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 3 (September 2011): G508—G518. http://dx.doi.org/10.1152/ajpgi.00066.2011.

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Altered profiles of gene expression reflect the reprogramming of intestinal epithelial cells during their maturation along the crypt-luminal axis. To focus on genes important in this process, and how they in turn are regulated, we identified 14 transcripts commonly downregulated in expression during lineage-specific maturation of the immortalized cell lines Caco-2 (absorptive), HT29Cl16E (goblet), and HT29Cl19A (secretory) induced by contact inhibition of growth or the short-chain fatty acid butyrate. One such gene, Mybl2 (Myb-related protein B), has been linked to the stem cell phenotype, and we report is also markedly suppressed in maturing cells along the crypt-luminal axis in vivo. Mybl2 is not significantly downregulated transcriptionally during colon cell maturation, but we identified a potential micro-RNA (miRNA)-binding sequence in the Mybl2 3′-untranslated region that mediates reporter gene suppression in differentiating colon cells. Accordingly, miRNAs predicted to bind this functional target are upregulated in differentiating colon epithelial cells in vitro and in vivo; expression of one of these, hsa-miR-365 (but not hsa-324–5p), suppresses Mybl2 protein expression in proliferating Caco-2 cells. These data demonstrate that miRNA silencing plays an important role in regulating gene expression in maturing colon epithelial cells, and that utilizing a target-centered approach, rather than profiling global miRNA expression, can identify physiologically relevant, functional miRNAs.

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Lim, Gah-Hyun, Se Won Kim, Jaihyunk Ryu, Si-Yong Kang, Jin-Baek Kim, and Sang Hoon Kim. "Upregulation of the MYB2 Transcription Factor is Associated with Increased Accumulation of Anthocyanin in the Leaves of Dendrobium bigibbum." International Journal of Molecular Sciences 21, no. 16 (August 6, 2020): 5653. http://dx.doi.org/10.3390/ijms21165653.

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Orchids with colorful leaves and flowers have significant ornamental value. Here, we used γ-irradiation-based mutagenesis to produce a Dendrobium bigibbum mutant that developed purple instead of the normal green leaves. RNA sequencing of the mutant plant identified 2513 differentially expressed genes, including 1870 up- and 706 downregulated genes. The purple leaf color of mutant leaves was associated with increased expression of genes that encoded key biosynthetic enzymes in the anthocyanin biosynthetic pathway. In addition, the mutant leaves also showed increased expression of several families of transcription factors including the MYB2 gene. Transient overexpression of D. biggibumMYB2 in Nicotiana benthamiana was associated with increased expression of endogenous anthocyanin biosynthesis genes. Interestingly, transient overexpression of orthologous MYB2 genes from other orchids did not upregulate expression of endogenous anthocyanin biosynthesis genes. Together, these results suggest that the purple coloration of D. biggibum leaves is at least associated with increased expression of the MYB2 gene, and the MYB2 orthologs from orchids likely function differently, regardless of their high level of similarity.

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Pugliesi, Claudio, Mariangela Salvini, and Marco Fambrini. "Isolation and molecular analysis of two R2R3-MYB genes from the sunflower (Helianthus annuus)." Botany 91, no. 10 (October 2013): 731–38. http://dx.doi.org/10.1139/cjb-2013-0071.

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MYB factors comprise one of the largest family of transcription factors (TFs) characterized by a highly conserved DNA-binding domain: the MYB domain. From the sunflower (Helianthus annuus L.) genome, we have isolated two R2R3-type MYB TFs (Ha-R2R3-MYB1 and Ha-R2R3-MYB2) that show homology with the functional domain of most R2R3-MYB proteins of other species. The R2 (53 amino acids) and R3 (51 amino acids) motifs of the sunflower MYB TFs contain typical amino acids, including a series of highly conserved tryptophan residues, which play a key role in sequence-specific DNA binding. In the MYB domain, both genes (Ha-R2R3-MYB1 and Ha-R2R3-MYB2) exhibit the highly conserved splicing arrangement of three exons and two introns. Using in situ hybridization, a weak level of Ha-R2R3-MYB1 transcription was uniformly spread in shoot apical meristem (SAM), as well as in axillary meristem (AM). By contrast, Ha-R2R3-MYB2 transcription was strongly restricted to a small domain within the boundary zone separating the SAM and the leaf primordia, suggesting that Ha-R2R3-MYB2 may be involved in an early step of AM development.

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Sun, Chin-Hung, Shih-Che Weng, Jui-Hsuan Wu, Szu-Yu Tung, Li-Hsin Su, Meng-Hsuan Lin, and Gilbert Aaron Lee. "DNA topoisomerase IIIβ promotes cyst generation by inducing cyst wall protein gene expression in Giardia lamblia." Open Biology 10, no. 2 (February 2020): 190228. http://dx.doi.org/10.1098/rsob.190228.

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Giardia lamblia causes waterborne diarrhoea by transmission of infective cysts. Three cyst wall proteins are highly expressed in a concerted manner during encystation of trophozoites into cysts. However, their gene regulatory mechanism is still largely unknown. DNA topoisomerases control topological homeostasis of genomic DNA during replication, transcription and chromosome segregation. They are involved in a variety of cellular processes including cell cycle, cell proliferation and differentiation, so they may be valuable drug targets. Giardia lamblia possesses a type IA DNA topoisomerase (TOP3β) with similarity to the mammalian topoisomerase IIIβ. We found that TOP3β was upregulated during encystation and it possessed DNA-binding and cleavage activity. TOP3β can bind to the cwp promoters in vivo using norfloxacin-mediated topoisomerase immunoprecipitation assays. We also found TOP3β can interact with MYB2, a transcription factor involved in the coordinate expression of cwp1-3 genes during encystation. Interestingly, overexpression of TOP3β increased expression of cwp1 - 3 and myb2 genes and cyst formation. Microarray analysis confirmed upregulation of cwp1-3 and myb2 genes by TOP3β. Mutation of the catalytically important Tyr residue, deletion of C-terminal zinc ribbon domain or further deletion of partial catalytic core domain reduced the levels of cleavage activity, cwp1-3 and myb2 gene expression, and cyst formation. Interestingly, some of these mutant proteins were mis-localized to cytoplasm. Using a CRISPR/Cas9 system for targeted disruption of top3β gene, we found a significant decrease in cwp1-3 and myb2 gene expression and cyst number. Our results suggest that TOP3β may be functionally conserved, and involved in inducing Giardia cyst formation.

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Yan, Xingxing, Ying Huang, Hui Song, Feng Chen, Qingliu Geng, Min Hu, Cheng Zhang, Xi Wu, Tingting Fan, and Shuqing Cao. "A MYB4-MAN3-Mannose-MNB1 signaling cascade regulates cadmium tolerance in Arabidopsis." PLOS Genetics 17, no. 6 (June 28, 2021): e1009636. http://dx.doi.org/10.1371/journal.pgen.1009636.

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Our previous studies showed that MAN3-mediated mannose plays an important role in plant responses to cadmium (Cd) stress. However, the underlying mechanisms and signaling pathways involved are poorly understood. In this study, we showed that an Arabidopsis MYB4-MAN3-Mannose-MNB1 signaling cascade is involved in the regulation of plant Cd tolerance. Loss-of-function of MNB1 (mannose-binding-lectin 1) led to decreased Cd accumulation and tolerance, whereas overexpression of MNB1 significantly enhanced Cd accumulation and tolerance. Consistently, expression of the genes involved in the GSH-dependent phytochelatin (PC) synthesis pathway (such as GSH1, GSH2, PCS1, and PCS2) was significantly reduced in the mnb1 mutants but markedly increased in the MNB1-OE lines in the absence or presence of Cd stress, which was positively correlated with Cd-activated PC synthesis. Moreover, we found that mannose is able to bind to the GNA-related domain of MNB1, and that mannose binding to the GNA-related domain of MNB1 is required for MAN3-mediated Cd tolerance in Arabidopsis. Further analysis showed that MYB4 directly binds to the promoter of MAN3 to positively regulate the transcript of MAN3 and thus Cd tolerance via the GSH-dependent PC synthesis pathway. Consistent with these findings, overexpression of MAN3 rescued the Cd-sensitive phenotype of the myb4 mutant but not the mnb1 mutant, whereas overexpression of MNB1 rescued the Cd-sensitive phenotype of the myb4 mutant. Taken together, our results provide compelling evidence that a MYB4-MAN3-Mannose-MNB1 signaling cascade regulates cadmium tolerance in Arabidopsis through the GSH-dependent PC synthesis pathway.

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Huang, Shao-Wei, Zi-Qi Lin, Szu-Yu Tung, Li-Hsin Su, Chun-Che Ho, Gilbert Aaron Lee, and Chin-Hung Sun. "A Novel Multiprotein Bridging Factor 1-Like Protein Induces Cyst Wall Protein Gene Expression and Cyst Differentiation in Giardia lamblia." International Journal of Molecular Sciences 22, no. 3 (January 29, 2021): 1370. http://dx.doi.org/10.3390/ijms22031370.

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The capacity to synthesize a protective cyst wall is critical for infectivity of Giardia lamblia. It is of interest to know the mechanism of coordinated synthesis of three cyst wall proteins (CWPs) during encystation, a differentiation process. Multiprotein bridging factor 1 (MBF1) gene family is a group of transcription coactivators that bridge various transcription factors. They are involved in cell growth and differentiation in yeast and animals, or in stress response in fungi and plants. We asked whether Giardia has MBF1-like genes and whether their products influence gene expression. BLAST searches of the Giardia genome database identified one gene encoding a putative MBF1 protein with a helix-turn-helix domain. We found that it can specifically bind to the AT-rich initiator promoters of the encystation-induced cwp1-3 and myb2 genes. MBF1 localized to cell nuclei and cytoplasm with higher expression during encystation. In addition, overexpression of MBF1 induced cwp1-3 and myb2 gene expression and cyst generation. Mutation of the helixes in the helix-turn-helix domain reduced cwp1-3 and myb2 gene expression and cyst generation. Chromatin immunoprecipitation assays confirmed the binding of MBF1 to the promoters with its binding sites in vivo. We also found that MBF1 can interact with E2F1, Pax2, WRKY, and Myb2 transcription factors that coordinately up-regulate the cwp genes during encystation. Using a CRISPR/Cas9 system for targeted disruption of mbf1 gene, we found a downregulation of cwp1-3 and myb2 genes and decrease of cyst generation. Our results suggest that MBF1 is functionally conserved and positively regulates Giardia cyst differentiation.

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Xu, Chengyan, Zixia He, Chao Lin, and Zhipeng Shen. "MiR-30b-5p inhibits proliferation and promotes apoptosis of medulloblastoma cells via targeting MYB proto-oncogene like 2 (MYBL2)." Journal of Investigative Medicine 68, no. 6 (July 19, 2020): 1179–85. http://dx.doi.org/10.1136/jim-2020-001354.

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Medulloblastoma (MB) is the most common malignant brain tumors among children. MiR-30b-5p is a potential tumor suppressor in a variety of human cancers. However, its expression and function in MB remain poorly understood. This study aimed to investigate the expression, role and regulatory mechanism of miR-30b-5p in MB. The expression of miR-30b-5p in MB tissues and cell lines was detected by real-time PCR. The effects of miR-30b-5p on cell proliferation and apoptosis were monitored by CCK-8 (Cell Counting Kit-8) assay, colony formation assay and flow cytometry, respectively. Bioinformatics database TargetScan predicted the target genes of miR-30b-5p. The interaction between miR-30b-5p and MYB proto-oncogene Like 2 (MYBL2) was determined by luciferase reporter gene assay. We demonstrated that the expression of miR-30b-5p was significantly downregulated in MB. Upregulated miR-30b-5p could inhibit the proliferation and induce apoptosis of MB.Moreover, overexpressed miR-30b-5p could increase the expression of BAX but decrease that of Bcl-2. Downregulated miR-30b-5p exerted the opposite effect. MYBL2 was proved to be the target gene of miR-30b-5p and was negatively regulated by miR-30b-5p. These results indicate that miR-30b-5p inhibits the progression of MB via targeting the expression of MYBL2.

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Ko, Jae-Heung, Won-Chan Kim, Joo-Yeol Kim, Sung-Ju Ahn, and Kyung-Hwan Han. "MYB46-Mediated Transcriptional Regulation of Secondary Wall Biosynthesis." Molecular Plant 5, no. 5 (September 2012): 961–63. http://dx.doi.org/10.1093/mp/sss076.

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Astbury, Katharine, Lynda McEvoy, Hayes Brian, Cathy Spillane, Orla Sheils, Cara Martin, and John J. O'Leary. "MYBL2 (B-MYB) in Cervical Cancer: Putative Biomarker." International Journal of Gynecologic Cancer 21, no. 2 (January 2011): 206–12. http://dx.doi.org/10.1097/igc.0b013e318205759f.

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Introduction:Cervical cancer is the second most common cancer affecting women worldwide. It is characterized by chromosomal aberrations and alteration in the expression levels of many cell cycle regulatory proteins.MYBL2is a member of theMYBproto-oncogene family that encodes DNA binding proteins. These proteins are involved in cell proliferation and control of cellular differentiation.Materials and Methods:Four established cervical cancer cell lines were examined and compared with normal cervix using gene expression profiling and comparative genomic hybridization, and results were correlated to identify potential novel cervical cancer biomarkers. Results were validated using TaqMan polymerase chain reaction, and the potential role of MYBL2 as a clinical biomarker was then evaluated by immunohistochemistry on 30 tissue samples.Results:MYBL2was found to be overexpressed in the cervical cancer cell lines by gene expression profiling, and this result was confirmed using TaqMan polymerase chain reaction. Analysis of comparative genomic hybridization data indicated that chromosome 20q13.1, which encodes theMYBL2gene, was amplified in the human papillomavirus (HPV) type 16-positive CaSki and SiHa cell lines but not in the HPV-18-positive HeLa or HPV-negative C33A cell lines.Discussion:Although MYBL2 staining was predominantly absent in normal cervical epithelium, strong staining (score of 2 or 3) was identified in all cases of cervical intraepithelial neoplasia, cervical glandular intraepithelial neoplasia, and invasive cancer on immunohistochemistry. In addition, strong staining of a population of diffusely scattered single cells is identified. We postulate that these may represent so-called cancer stem-like cells.

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Babak, O. G., S. I. Ignatova, N. A. Golubkina, N. A. Nekrashevich, N. V. Anisimova, T. V. Nikitinskaya, K. K. Yatsevich, and A. V. Kilchevsky. "Analysis of SlMYB12 gene polymorphism determining chalcone-naringenin biosynthesis in the skin of tomato fruits and its effect on the lycopene accumulation." Doklady of the National Academy of Sciences of Belarus 64, no. 6 (December 31, 2020): 702–12. http://dx.doi.org/10.29235/1561-8323-2020-64-6-702-712.

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Efficiency in detecting of tomato forms with no chalcone-naringenin flavonoid in pink-fruited and yellow-fruited forms was evaluated using DNA markers for various polymorphisms of the SlMYB12 gene. The closest relationship between a phenotype with the transparent skin of fruits and a deletion in the promoter region of the SlMYB12 gene was shown. The highest efficiency in the detection of the recessive y allele of the regulatory SlMYB12 gene, leading to the chalcone-naringenin synthesis disruption and skin transparency, was established by a combination of markers MYB12-603delaF1/603del-aR6 (Myb-603del aF1/R6) and MYB12-603del-aF1/603del-aR5 (Myb12 aF1/R5). Fruit coloration peculiarities were shown depending on a combination of the structural alleles of a carotenoid biosynthesis pathway and SlMYB12 gene alleles. A combination of this y allele with the alleles of the gene of the lycopene-β-cyclase beta (b) and old gold crimson (ogc ) allows selecting pink and raspberry forms respectively. In tomato accessions with yellow and orange fruits, the y allele provides pale shades of the main coloration determined by carotenoid biosynthesis genes (yellow flesh (r), tangerine (t), Beta (B)). The presence of SNP T → C of the SlMYB12 gene (171476848 position of chromosome 1) was identified in 80 % of accessions with the transparent skin of fruits of the evaluated collection. The effect of the recessive y allele of the SlMYB12 gene on an increase in the lycopene concentration of tomato fruits in a combination with b, ogc alleles was shown. Using MAC methods by fruit quality genes, including the SlMYB12 gene, the cherry tomato variety Malinovyj koktel with a high lycopene accumulation was developed and included in the State Register

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Babak, O. G., S. I. Ignatova, N. A. Golubkina, N. A. Nekrashevich, N. V. Anisimova, T. V. Nikitinskaya, K. K. Yatsevich, and A. V. Kilchevsky. "Analysis of SlMYB12 gene polymorphism determining chalcone-naringenin biosynthesis in the skin of tomato fruits and its effect on the lycopene accumulation." Doklady of the National Academy of Sciences of Belarus 64, no. 6 (December 31, 2020): 702–12. http://dx.doi.org/10.29235/1561-8323-2020-64-6-702-712.

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Efficiency in detecting of tomato forms with no chalcone-naringenin flavonoid in pink-fruited and yellow-fruited forms was evaluated using DNA markers for various polymorphisms of the SlMYB12 gene. The closest relationship between a phenotype with the transparent skin of fruits and a deletion in the promoter region of the SlMYB12 gene was shown. The highest efficiency in the detection of the recessive y allele of the regulatory SlMYB12 gene, leading to the chalcone-naringenin synthesis disruption and skin transparency, was established by a combination of markers MYB12-603delaF1/603del-aR6 (Myb-603del aF1/R6) and MYB12-603del-aF1/603del-aR5 (Myb12 aF1/R5). Fruit coloration peculiarities were shown depending on a combination of the structural alleles of a carotenoid biosynthesis pathway and SlMYB12 gene alleles. A combination of this y allele with the alleles of the gene of the lycopene-β-cyclase beta (b) and old gold crimson (ogc ) allows selecting pink and raspberry forms respectively. In tomato accessions with yellow and orange fruits, the y allele provides pale shades of the main coloration determined by carotenoid biosynthesis genes (yellow flesh (r), tangerine (t), Beta (B)). The presence of SNP T → C of the SlMYB12 gene (171476848 position of chromosome 1) was identified in 80 % of accessions with the transparent skin of fruits of the evaluated collection. The effect of the recessive y allele of the SlMYB12 gene on an increase in the lycopene concentration of tomato fruits in a combination with b, ogc alleles was shown. Using MAC methods by fruit quality genes, including the SlMYB12 gene, the cherry tomato variety Malinovyj koktel with a high lycopene accumulation was developed and included in the State Register

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Shi, Dachuan, Angyan Ren, Xianfeng Tang, Guang Qi, Zongchang Xu, Guohua Chai, Ruibo Hu, Gongke Zhou, and Yingzhen Kong. "MYB52 Negatively Regulates Pectin Demethylesterification in Seed Coat Mucilage." Plant Physiology 176, no. 4 (February 9, 2018): 2737–49. http://dx.doi.org/10.1104/pp.17.01771.

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Zhang, Ping, Ruling Wang, Qiong Ju, Weiqiang Li, Lam-Son Phan Tran, and Jin Xu. "The R2R3-MYB Transcription Factor MYB49 Regulates Cadmium Accumulation." Plant Physiology 180, no. 1 (February 19, 2019): 529–42. http://dx.doi.org/10.1104/pp.18.01380.

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Ramírez, Vicente, Astrid Agorio, Alberto Coego, Javier García-Andrade, M. José Hernández, Begoña Balaguer, Pieter B. F. Ouwerkerk, Ignacio Zarra, and Pablo Vera. "MYB46 Modulates Disease Susceptibility to Botrytis cinerea in Arabidopsis." Plant Physiology 155, no. 4 (January 31, 2011): 1920–35. http://dx.doi.org/10.1104/pp.110.171843.

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Liang, Gang, Hua He, Yang Li, Qin Ai, and Diqiu Yu. "MYB82 functions in regulation of trichome development in Arabidopsis." Journal of Experimental Botany 65, no. 12 (May 6, 2014): 3215–23. http://dx.doi.org/10.1093/jxb/eru179.

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Clarke, M., S. Dumon, C. Ward, R. Jäger, S. Freeman, B. Dawood, L. Sheriff, et al. "MYBL2 haploinsufficiency increases susceptibility to age-related haematopoietic neoplasia." Leukemia 27, no. 3 (August 22, 2012): 661–70. http://dx.doi.org/10.1038/leu.2012.241.

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Hsu, Hong-Ming, Yu Lee, Dharmu Indra, Shu-Yi Wei, Hsing-Wei Liu, Lung-Chun Chang, Chinpan Chen, Shiou-Jeng Ong, and Jung-Hsiang Tai. "Iron-Inducible Nuclear Translocation of a Myb3 Transcription Factor in the Protozoan Parasite Trichomonas vaginalis." Eukaryotic Cell 11, no. 12 (October 5, 2012): 1441–50. http://dx.doi.org/10.1128/ec.00190-12.

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ABSTRACTInTrichomonas vaginalis, a novel nuclear localization signal spanning the folded R2R3 DNA-binding domain of a Myb2 protein was previously identified. To study whether a similar signal is used for nuclear translocation by other Myb proteins, nuclear translocation of Myb3 was examined in this report. When overexpressed, hemagglutinin-tagged Myb3 was localized to nuclei of transfected cells, with a cellular distribution similar to that of endogenous Myb3. Fusion to a bacterial tetracycline repressor, R2R3, of Myb3 that spans amino acids (aa) 48 to 156 was insufficient for nuclear translocation of the fusion protein, unless its C terminus was extended to aa 167. The conserved isoleucine in helix 2 of R2R3, which is important for Myb2's structural integrity in maintaining DNA-binding activity and nuclear translocation, was also vital for the former activity of Myb3, but less crucial for the latter. Sequential nuclear influx and efflux of Myb3, which require further extension of the nuclear localization signal to aa 180, were immediately induced after iron repletion. Sequence elements that regulate nuclear translocation with cytoplasmic retention, nuclear influx, and nuclear efflux were identified within the C-terminal tail. These results suggest that the R2R3 DNA-binding domain also serves as a common module for the nuclear translocation of both Myb2 and Myb3, but there are intrinsic differences between the two nuclear localization signals.

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Luo, Zhiwen, Xinyu Bi, and Xingang Bi. "Role of DNA polymerases family members in cancer: The pan-cancer perspective." Journal of Clinical Oncology 39, no. 3_suppl (January 20, 2021): 475. http://dx.doi.org/10.1200/jco.2021.39.3_suppl.475.

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475 Background: DNA polymerases family (DNA pols) has a lengthy reported significant influence on the initiation, development, and progress of cancer. However, the pan-cancer value of whole family members was poorly done. Our study intends to demonstrate the expression pattern and clinical cancer value of DNA pols members as prognostic biomarkers and a therapeutic target of pan-cancer. Methods: Comprehensive bioinformatics analyses were done using data from TCGA and CCLE. MultiCox regression was done to select tumor prognosis-related members. Nomogram was constructed to predict the overall survival (OS) across cancer patients. Transcription factor, GO, IPA, and GSEA enrichments were done to explore regulatory mechanisms and functions. Results: A total of 22 DNA pols were identified to have a potential to diagnostic value, and 10 DNA pols have a pan-cancer prognostic value under various stages, and cancer type, among which overexpression of 6 DNA-pols (POLA2, POLD1, POLD2, POLE2, POLE4, and POLQ) was found to be significantly related to worse outcomes regarding OS, while 4 DNA-pols (POLH, POLL, POLN, and REV1) significantly related to better outcomes. A 5-DNA pols based risk score (POLQ, POLD2, POLL, POLH, and REV1) was generated by MultiCox regression with a nomogram validated an accurate predictive efficacy. MYB Proto-Oncogene Like 2 (MYBL2) was identified as transcription factors of prognostic DNA pols in pan-cancer, and IPA mimic experiment reveals inhibiting MYBL2 could be a drug target to recover and balance the dysregulated expression pattern of DNA pols in pan-cancer. GO, IPA, and GSEA enrichments revealed functions and pathways altered by DNA pols in cancer, and the results were supported by pan-cancer cell sequencing data. Conclusions: DNA pols have a pan-cancer clinical value and can work as potential prognostic biomarkers. Furthermore, MYBL2 could be a drug target for pan-cancer.

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Wang, Xiao‐Chen, Jie Wu, Meng‐Ling Guan, Cui‐Huan Zhao, Pan Geng, and Qiao Zhao. "Arabidopsis MYB4 plays dual roles in flavonoid biosynthesis." Plant Journal 101, no. 3 (December 22, 2019): 637–52. http://dx.doi.org/10.1111/tpj.14570.

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Xu, Sutie, Sarah L. Ottinger, Sean M. Schaeffer, Jennifer M. DeBruyn, C. Neal Stewart, Mitra Mazarei, and Sindhu Jagadamma. "Effects of field-grown transgenic switchgrass carbon inputs on soil organic carbon cycling." PeerJ 7 (October 16, 2019): e7887. http://dx.doi.org/10.7717/peerj.7887.

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Genetic engineering has been used to decrease the lignin content and to change the lignin composition of switchgrass (Panicum virgatum L.) to decrease cell wall recalcitrance to enable more efficient cellulosic biofuel production. Previous greenhouse and field studies showed that downregulation of the gene encoding switchgrass caffeic acid O-methyltransferase (COMT) and overexpression of the switchgrass PvMYB4 (MYB4) gene effectively improved ethanol yield. To understand potential environmental impacts of cultivating these transgenic bioenergy crops in the field, we quantified the effects of field cultivation of transgenic switchgrass on soil organic carbon (SOC) dynamics. Total and active SOC as well as soil respiration were measured in soils grown with two COMT-downregulated transgenic lines (COMT2 and COMT3), three MYB4-overexpressed transgenic lines (L1, L6, and L8), and their corresponding non-transgenic controls. No differences in total SOC, dissolved organic carbon (DOC), and permanganate oxidizable carbon (POXC) were detected between transgenic and non-transgenic treatments for both COMT (10.4–11.1 g kg−1 for SOC, 60.0–64.8 mg kg−1 for DOC, and 299–384 mg kg−1 for POXC) and MYB4 lines (6.89–8.21 g kg−1 for SOC, 56.0–61.1 mg kg−1 for DOC, and 177–199 mg kg−1 for POXC). Soil CO2-carbon (CO2-C) production from the COMT2 transgenic line was not significantly different from its non-transgenic control. In contrast, the COMT3 transgenic line had greater soil CO2-C production than its non-transgenic control (210 vs. 165 µg g−1) after 72 days of laboratory incubation. Combining the improvement in ethanol yield and biomass production reported in previous studies with negligible change in SOC and soil respiration, COMT2 could be a better biofuel feedstock than COMT3 for environmental conservation and cost-effective biofuel production. On the other hand, MYB4 transgenic line L8 produced more biomass and total ethanol per hectare while it released more CO2-C than the control (253 vs. 207 µg g−1). Long-term in situ monitoring of transgenic switchgrass systems using a suite of soil and environmental variables is needed to determine the sustainability of growing genetically modified bioenergy crops.

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Jia, Yongxu, Yaping Gao, Jing Li, Zhiwei Chang, Jie Yan, and Yanru Qin. "Prognostic implications of MYBL2 in resected Chinese gastric adenocarcinoma patients." OncoTargets and Therapy Volume 12 (February 2019): 1129–35. http://dx.doi.org/10.2147/ott.s188820.

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Dubos, Christian, José Le Gourrierec, Antoine Baudry, Gunnar Huep, Elodie Lanet, Isabelle Debeaujon, Jean-Marc Routaboul, Alessandro Alboresi, Bernd Weisshaar, and Loïc Lepiniec. "MYBL2 is a new regulator of flavonoid biosynthesis inArabidopsis thaliana." Plant Journal 55, no. 6 (September 2008): 940–53. http://dx.doi.org/10.1111/j.1365-313x.2008.03564.x.

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Bayley, Rachel, Ciara Ward, and Paloma Garcia. "MYBL2 amplification in breast cancer: Molecular mechanisms and therapeutic potential." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1874, no. 2 (December 2020): 188407. http://dx.doi.org/10.1016/j.bbcan.2020.188407.

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Vera, Olga, Ilah Bok, Neel Jasani, Koji Nakamura, Xiaonan Xu, Nicol Mecozzi, Ariana Angarita, Kaizhen Wang, Kenneth Y. Tsai, and Florian A. Karreth. "A MAPK/miR-29 Axis Suppresses Melanoma by Targeting MAFG and MYBL2." Cancers 13, no. 6 (March 19, 2021): 1408. http://dx.doi.org/10.3390/cancers13061408.

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The miR-29 family of microRNAs is encoded by two clusters, miR-29b1~a and miR-29b2~c, and is regulated by several oncogenic and tumor suppressive stimuli. While in vitro evidence suggests a tumor suppressor role for miR-29 in melanoma, the mechanisms underlying its deregulation and contribution to melanomagenesis have remained elusive. Using various in vitro systems, we show that oncogenic MAPK signaling paradoxically stimulates transcription of pri-miR-29b1~a and pri-miR-29b2~c, the latter in a p53-dependent manner. Expression analyses in melanocytes, melanoma cells, nevi, and primary melanoma revealed that pri-miR-29b2~c levels decrease during melanoma progression. Inactivation of miR-29 in vivo with a miRNA sponge in a rapid melanoma mouse model resulted in accelerated tumor development and decreased overall survival, verifying tumor suppressive potential of miR-29 in melanoma. Through integrated RNA sequencing, target prediction, and functional assays, we identified the transcription factors MAFG and MYBL2 as bona fide miR-29 targets in melanoma. Our findings suggest that attenuation of miR-29b2~c expression promotes melanoma development, at least in part, by derepressing MAFG and MYBL2.

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Xiao, Ruixue, Chong Zhang, Xiaorui Guo, Hui Li, and Hai Lu. "MYB Transcription Factors and Its Regulation in Secondary Cell Wall Formation and Lignin Biosynthesis during Xylem Development." International Journal of Molecular Sciences 22, no. 7 (March 30, 2021): 3560. http://dx.doi.org/10.3390/ijms22073560.

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The secondary wall is the main part of wood and is composed of cellulose, xylan, lignin, and small amounts of structural proteins and enzymes. Lignin molecules can interact directly or indirectly with cellulose, xylan and other polysaccharide molecules in the cell wall, increasing the mechanical strength and hydrophobicity of plant cells and tissues and facilitating the long-distance transportation of water in plants. MYBs (v-myb avian myeloblastosis viral oncogene homolog) belong to one of the largest superfamilies of transcription factors, the members of which regulate secondary cell-wall formation by promoting/inhibiting the biosynthesis of lignin, cellulose, and xylan. Among them, MYB46 and MYB83, which comprise the second layer of the main switch of secondary cell-wall biosynthesis, coordinate upstream and downstream secondary wall synthesis-related transcription factors. In addition, MYB transcription factors other than MYB46/83, as well as noncoding RNAs, hormones, and other factors, interact with one another to regulate the biosynthesis of the secondary wall. Here, we discuss the biosynthesis of secondary wall, classification and functions of MYB transcription factors and their regulation of lignin polymerization and secondary cell-wall formation during wood formation.

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Miyagi-Shiohira, Chika, Issei Saitoh, Masami Watanabe, and Hirofumi Noguchi. "Gene Expression in Pancreatic Cancer-Like Cells and Induced Pancreatic Stem Cells Generated by Transient Overexpression of Reprogramming Factors." Journal of Clinical Medicine 10, no. 3 (January 25, 2021): 454. http://dx.doi.org/10.3390/jcm10030454.

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We previously reported that transient overexpression of reprogramming factors can be used to generate induced pluripotent stem (iPS) cells, induced tissue-specific stem (iTS) cells, and fibroblast-like (iF) cells from pancreatic tissue. iF cells have tumorigenic ability and behave similarly to pancreatic cancer cells. In this study, we analyzed gene expression in iF cells and iTS-P cells (iTS cells from pancreatic tissue) via microarray analysis and quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The expression levels of the Mybl2 and Lyn genes, which are reported to be oncogenes, were significantly higher in iF cells than in iTS-P cells. The expression level of Nestin, which is expressed in not only pancreatic progenitor cells but also pancreatic ductal adenocarcinomas, was also higher in iF cells than in iTS-P cells. Itgb6 and Fgf13, which are involved in the pathogenesis of diseases such as cancer, exhibited higher expression levels in iF cells than in iTS-P cells. Unexpectedly, the expression levels of genes related to epithelial-mesenchymal transition (EMT), except Bmp4, were lower in iF cells than in iTS-P cells. These data suggest that the Mybl2, Lyn, Nestin, Itgb6, and Fgf13 genes could be important biomarkers to distinguish iTS-P cells from iF cells.

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Noben-Trauth, Konrad, Neal G. Copeland, Debra J. Gilbert, Nancy A. Jenkins, Gonosuke Sonoda, Joseph R. Testa, and Karl-Heinz Klempnauer. "Mybl2(Bmyb) Maps to Mouse Chromosome 2 and Human Chromosome 20q13.1." Genomics 35, no. 3 (August 1996): 610–12. http://dx.doi.org/10.1006/geno.1996.0408.

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Palmer, Christine M., Maria N. Hindt, Holger Schmidt, Stephan Clemens, and Mary Lou Guerinot. "MYB10 and MYB72 Are Required for Growth under Iron-Limiting Conditions." PLoS Genetics 9, no. 11 (November 21, 2013): e1003953. http://dx.doi.org/10.1371/journal.pgen.1003953.

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Thomas, Carla, Cleo Robinson, Ben Dessauvagie, Benjamin Wood, Greg Sterrett, Jennet Harvey, and Benhur Amanuel. "Expression of proliferation genes in formalin-fixed paraffin-embedded (FFPE) tissue from breast carcinomas. Feasibility and relevance for a routine histopathology laboratory." Journal of Clinical Pathology 70, no. 1 (May 27, 2016): 25–32. http://dx.doi.org/10.1136/jclinpath-2016-203786.

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AimBreast carcinoma proliferative activity, histological grade and commercial molecular tests are all important in prognostication and treatment. There is a particular need for improved, standardised techniques for subclassification of grade 2 breast cancers into low-risk and high-risk prognostic groups. In this study we investigated whether gene expression profiling of five proliferation genes was feasible using breast cancer tissue in a clinical setting and whether these profiles could enhance pathological assessment.MethodsExpression of five proliferation gene mRNAs; Ki-67, STK 15, CCNB1, CCND1 and MYBL2, was quantified in 27 breast carcinomas and compared with Ki-67 proliferation index (PI) and Nottingham mitotic score.ResultsExpression of Ki-67, STK15 and MYBL2 mRNA showed moderate Spearman's correlation with Ki-67 PI (p<0.01), but CCND1 and CCNB1 showed weak, non-significant correlation. Individual gene expression did not associate with mitotic score but combined mRNA expression correlated with both Ki-67 PI (p=0.018) and mitotic score (p=0.03; 0.007).ConclusionsThis study confirms mRNA analysis in breast carcinoma formalin-fixed, paraffin-embedded samples is feasible and suggests gene expression profiling, using a small set of five proliferation genes, has potential in aiding histological grading or assessment of proliferative activity of breast cancers. To fully evaluate the clinical applicability of this approach, a larger cohort study with long-term follow-up data is required.

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Huang, Yu-Chang, Li-Hsin Su, Gilbert A. Lee, Pei-Wei Chiu, Chao-Cheng Cho, Jeng-You Wu, and Chin-Hung Sun. "Regulation of Cyst Wall Protein Promoters by Myb2 inGiardia lamblia." Journal of Biological Chemistry 283, no. 45 (September 3, 2008): 31021–29. http://dx.doi.org/10.1074/jbc.m805023200.

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Kim, Juri, Mee Young Shin, and Soon-Jung Park. "Functional Identification of a Nuclear Localization Signal of MYB2 Protein in Giardia lamblia." Korean Journal of Parasitology 58, no. 6 (December 29, 2020): 675–79. http://dx.doi.org/10.3347/kjp.2020.58.6.675.

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MYB2 protein was identified as a transcription factor that showed encystation-induced expression in Giardia lamblia. Although nuclear import is essential for the functioning of a transcription factor, an evident nuclear localization signal (NLS) of G. lamblia MYB2 (GlMYB2) has not been defined. Based on putative GlMYB2 NLSs predicted by 2 programs, a series of plasmids expressing hemagglutinin (HA)-tagged GlMYB2 from the promoter of G. lamblia glutamate dehydrogenase were constructed and transfected into Giardia trophozoites. Immunofluorescence assays using anti-HA antibodies indicated that GlMYB2 amino acid sequence #507–#530 was required for the nuclear localization of GlMYB2, and this sequence was named as NLSGlMYB2. We further verified this finding by demonstrating the nuclear location of a protein obtained by the fusion of NLSGlMYB2 and G. lamblia glyceraldehyde 3-phosphate dehydrogenase, a non-nuclear protein. Our data on GlMYB2 will expand our understanding on NLSs functioning in G. lamblia.

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Papetti, Michael, and Leonard H. Augenlicht. "MYBL2, a link between proliferation and differentiation in maturing colon epithelial cells." Journal of Cellular Physiology 226, no. 3 (December 28, 2010): 785–91. http://dx.doi.org/10.1002/jcp.22399.

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Shi, Hong, Melanie Bevier, Robert Johansson, Kerstin Enquist-Olsson, Roger Henriksson, Kari Hemminki, Per Lenner, and Asta Försti. "Prognostic impact of polymorphisms in the MYBL2 interacting genes in breast cancer." Breast Cancer Research and Treatment 131, no. 3 (October 26, 2011): 1039–47. http://dx.doi.org/10.1007/s10549-011-1826-2.

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Journal articles on the topic 'MYB42'

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