Статті в журналах: "PSKH1"

1

Brede, G. "PSKH1, a novel splice factor compartment-associated serine kinase." Nucleic Acids Research 30, no. 23 (December 1, 2002): 5301–9. http://dx.doi.org/10.1093/nar/gkf648.

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2

Brede, Gaute, Jorun Solheim, Espen Stang, and Hans Prydz. "Mutants of the protein serine kinase PSKH1 disassemble the Golgi apparatus." Experimental Cell Research 291, no. 2 (December 10, 2003): 299–312. http://dx.doi.org/10.1016/j.yexcr.2003.07.009.

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3

Firth, Neville, Sumalee Apisiridej, Tracey Berg, Brendon A. O'Rourke, Steve Curnock, Keith G. H. Dyke, and Ronald A. Skurray. "Replication of Staphylococcal Multiresistance Plasmids." Journal of Bacteriology 182, no. 8 (April 15, 2000): 2170–78. http://dx.doi.org/10.1128/jb.182.8.2170-2178.2000.

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ABSTRACT Based on structural and functional properties, three groups of large staphylococcal multiresistance plasmids have been recognized, viz., the pSK1 family, pSK41-like conjugative plasmids, and β-lactamase–heavy-metal resistance plasmids. Here we describe an analysis of the replication functions of a representative of each of these plasmid groups. The replication initiation genes from theStaphylococcus aureus plasmids pSK1, pSK41, and pI9789::Tn552 were found to be related to each other and to the Staphylococcus xylosus plasmid pSX267 and are also related to rep genes of several plasmids from other gram-positive genera. Nucleotide sequence similarity between pSK1 and pI9789::Tn552 extended beyond theirrep genes, encompassing upstream divergently transcribed genes, orf245 and orf256, respectively. Our analyses revealed that genes encoding proteins related to the deducedorf245 product are variously represented, in several types of organization, on plasmids possessing six seemingly evolutionarily distinct types of replication initiation genes and including both theta-mode and rolling-circle replicons. Construction of minireplicons and subsequent functional analysis demonstrated that orf245is required for the segregational stability of the pSK1 replicon. In contrast, no gene equivalent to orf245 is evident on the conjugative plasmid pSK41, and a minireplicon encoding only the pSK41 rep gene was found to exhibit a segregational stability approaching that of the parent plasmid. Significantly, the results described establish that many of the large multiresistance plasmids that have been identified in clinical staphylococci, which were formerly presumed to be unrelated, actually utilize an evolutionarily related theta-mode replication system.

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4

Brede, Gaute, Jorun Solheim, Gunhild Tröen, and Hans Prydz. "Characterization of PSKH1, a Novel Human Protein Serine Kinase with Centrosomal, Golgi, and Nuclear Localization." Genomics 70, no. 1 (November 2000): 82–92. http://dx.doi.org/10.1006/geno.2000.6365.

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5

Dai, Yiping, Liping Xie, Xunhao Xiong, Lei Chen, Weimin Fan, and Rongqing Zhang. "Cloning and Characterization of a Homologous Ca2+/calmodulin-dependent protein kinase PSKH1 from pearl oyster pinctada fucata." Tsinghua Science and Technology 10, no. 4 (August 2005): 504–11. http://dx.doi.org/10.1016/s1007-0214(05)70108-5.

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6

Fan, Danyang, Yilong Yao, Yanwen Liu, Chao Yan, Fanqinyu Li, Shilong Wang, Mei Yu, Bingkun Xie, and Zhonglin Tang. "Regulation of myo-miR-24-3p on the Myogenesis and Fiber Type Transformation of Skeletal Muscle." Genes 15, no. 3 (February 21, 2024): 269. http://dx.doi.org/10.3390/genes15030269.

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Skeletal muscle plays critical roles in providing a protein source and contributing to meat production. It is well known that microRNAs (miRNAs) exert important effects on various biological processes in muscle, including cell fate determination, muscle fiber morphology, and structure development. However, the role of miRNA in skeletal muscle development remains incompletely understood. In this study, we observed a critical miRNA, miR-24-3p, which exhibited higher expression levels in Tongcheng (obese-type) pigs compared to Landrace (lean-type) pigs. Furthermore, we found that miR-24-3p was highly expressed in the dorsal muscle of pigs and the quadriceps muscle of mice. Functionally, miR-24-3p was found to inhibit proliferation and promote differentiation in muscle cells. Additionally, miR-24-3p was shown to facilitate the conversion of slow muscle fibers to fast muscle fibers and influence the expression of GLUT4, a glucose transporter. Moreover, in a mouse model of skeletal muscle injury, we demonstrated that overexpression of miR-24-3p promoted rapid myogenesis and contributed to skeletal muscle regeneration. Furthermore, miR-24-3p was found to regulate the expression of target genes, including Nek4, Pim1, Nlk, Pskh1, and Mapk14. Collectively, our findings provide evidence that miR-24-3p plays a regulatory role in myogenesis and fiber type conversion. These findings contribute to our understanding of human muscle health and have implications for improving meat production traits in livestock.

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7

de Souza, João V., Matthew Kondal, Piotr Zaborniak, Ryland Cairns, and Agnieszka K. Bronowska. "Controlling the Heterodimerisation of the Phytosulfokine Receptor 1 (PSKR1) via Island Loop Modulation." International Journal of Molecular Sciences 22, no. 4 (February 11, 2021): 1806. http://dx.doi.org/10.3390/ijms22041806.

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Phytosulfokine (PSK) is a phytohormone responsible for cell-to-cell communication in plants, playing a pivotal role in plant development and growth. The binding of PSK to its cognate receptor, PSKR1, is modulated by the formation of a binding site located between a leucine-rich repeat (LRR) domain of PSKR1 and the loop located in the receptor’s island domain (ID). The atomic resolution structure of the extracellular PSKR1 bound to PSK has been reported, however, the intrinsic dynamics of PSK binding and the architecture of the PSKR1 binding site remain to be understood. In this work, we used atomistic molecular dynamics (MD) simulations and free energy calculations to elucidate how the PSKR1 island domain (ID) loop forms and binds PSK. Moreover, we report a novel “druggable” binding site which could be exploited for the targeted modulation of the PSKR1-PSK binding by small molecules. We expect that our results will open new ways to modulate the PSK signalling cascade via small molecules, which can result in new crop control and agricultural applications.

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8

Pollet, Rebecca M., James D. Ingle, Jeff P. Hymes, Thomas C. Eakes, Karina Yui Eto, Stephen M. Kwong, Joshua P. Ramsay, Neville Firth, and Matthew R. Redinbo. "Processing of Nonconjugative Resistance Plasmids by Conjugation Nicking Enzyme of Staphylococci." Journal of Bacteriology 198, no. 6 (January 4, 2016): 888–97. http://dx.doi.org/10.1128/jb.00832-15.

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ABSTRACTAntimicrobial resistance inStaphylococcus aureuspresents an increasing threat to human health. This resistance is often encoded on mobile plasmids, such as pSK41; however, the mechanism of transfer of these plasmids is not well understood. In this study, we first examine key protein-DNA interactions formed by the relaxase enzyme, NES, which initiates and terminates the transfer of the multidrug resistance plasmid pSK41. Two loops on the NES protein, hairpin loops 1 and 2, form extensive contacts with the DNA hairpin formed at theoriTregion of pSK41, and here we establish that these contacts are essential for proper DNA cleavage and religation by the full 665-residue NES proteinin vitro. Second, pSK156 and pCA347 are nonconjugativeStaphylococcus aureusplasmids that contain sequences similar to theoriTregion of pSK41 but differ in the sequence predicted to form a DNA hairpin. We show that pSK41-encoded NES is able to bind, cleave, and religate theoriTsequences of these nonconjugative plasmidsin vitro. Although pSK41 could mobilize a coresident plasmid harboring its cognateoriT, it was unable to mobilize plasmids containing the pSK156 and pCA347 variantoriTmimics, suggesting that an accessory protein like that previously shown to confer specificity in the pWBG749 system may also be involved in transmission of plasmids containing a pSK41-likeoriT. These data indicate that the conjugative relaxase intransmechanism recently described for the pWBG749 family of plasmids also applies to the pSK41 family of plasmids, further heightening the potential significance of this mechanism in the horizontal transfer of staphylococcal plasmids.IMPORTANCEUnderstanding the mechanism of antimicrobial resistance transfer in bacteria such asStaphylococcus aureusis an important step toward potentially slowing the spread of antimicrobial-resistant infections. This work establishes protein-DNA interactions essential for the transfer of theStaphylococcus aureusmultiresistance plasmid pSK41 by its relaxase, NES. This enzyme also processed variantoriT-like sequences found on numerous plasmids previously considered nontransmissible, suggesting that in conjunction with an uncharacterized accessory protein, these plasmids may be transferred horizontally via a relaxase intransmechanism. These findings have important implications for our understanding of staphylococcal resistance plasmid evolution.

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9

Zhu, Wenming, Nancye Clark, and Jean B. Patel. "pSK41-Like Plasmid Is Necessary for Inc18-LikevanAPlasmid Transfer from Enterococcus faecalis to Staphylococcus aureusIn Vitro." Antimicrobial Agents and Chemotherapy 57, no. 1 (October 22, 2012): 212–19. http://dx.doi.org/10.1128/aac.01587-12.

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ABSTRACTVancomycin-resistantStaphylococcus aureus(VRSA) is thought to result from thein vivoconjugative transfer of avanAplasmid from anEnterococcussp. toS. aureus. We studied bacterial isolates from VRSA cases that occurred in the United States to identify microbiological factors which may contribute to this plasmid transfer. First, vancomycin-susceptible, methicillin-resistantS. aureus(MRSA) isolates from five VRSA cases were tested for their ability to accept foreign DNA by conjugation in mating experiments withEnterococcus faecalisJH2-2 containing pAM378, a pheromone-response conjugative plasmid. All of the MRSA isolates accepted the plasmid DNA with similar transfer efficiencies (∼10−7/donor CFU) except for one isolate, MRSA8, for which conjugation was not successful. The MRSA isolates were also tested as recipients in mating experiments between anE. faecalisisolate with an Inc18-likevanAplasmid that was isolated from a VRSA case patient. Conjugative transfer was successful for 3/5 MRSA isolates. Successful MRSA recipients carried a pSK41-like plasmid, a staphylococcal conjugative plasmid, whereas the two unsuccessful MRSA recipients did not carry pSK41. The transfer of a pSK41-like plasmid from a successful MRSA recipient to the two unsuccessful recipients resulted in conjugal transfer of the Inc18-likevanAplasmid fromE. faecalisat a frequency of 10−7/recipient CFU. In addition, conjugal transfer could be achieved for pSK41-negative MRSA in the presence of a cell-free culture filtrate fromS. aureuscarrying a pSK41-like plasmid at a frequency of 10−8/recipient CFU. These results indicated that a pSK41-like plasmid can facilitate the transfer of an Inc18-likevanAplasmid fromE. faecalistoS. aureus, possibly via an extracellular factor produced by pSK41-carrying isolates.

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10

Kirienko, Anna N., Nadezhda A. Vishnevskaya, Anna B. Kitaeva, Oksana Yu Shtark, Polina Yu Kozyulina, Richard Thompson, Marion Dalmais, Abdelhafid Bendahmane, Igor A. Tikhonovich, and Elena A. Dolgikh. "Structural Variations in LysM Domains of LysM-RLK PsK1 May Result in a Different Effect on Pea–Rhizobial Symbiosis Development." International Journal of Molecular Sciences 20, no. 7 (April 1, 2019): 1624. http://dx.doi.org/10.3390/ijms20071624.

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Lysin-motif receptor-like kinase PsK1 is involved in symbiosis initiation and the maintenance of infection thread (IT) growth and bacterial release in pea. We verified PsK1 specificity in relation to the Nod factor structure using k1 and rhizobial mutants. Inoculation with nodO and nodE nodO mutants significantly reduced root hair deformations, curling, and the number of ITs in k1-1 and k1-2 mutants. These results indicated that PsK1 function may depend on Nod factor structures. PsK1 with replacement in kinase domain and PsSYM10 co-production in Nicotiana benthamiana leaves did not induce a hypersensitive response (HR) because of the impossibility of signal transduction into the cell. Replacement of P169S in LysM3 domain of PsK1 disturbed the extracellular domain (ECD) interaction with PsSYM10′s ECD in Y2H system and reduced HR during the co-production of full-length PsK1 and PsSYM0 in N. benthamiana. Lastly, we explored the role of PsK1 in symbiosis with arbuscular mycorrhizal (AM) fungi; no significant differences between wild-type plants and k1 mutants were found, suggesting a specific role of PsK1 in legume–rhizobial symbiosis. However, increased sensitivity to a highly aggressive Fusarium culmorum strain was found in k1 mutants compared with the wild type, which requires the further study of the role of PsK1 in immune response regulation.

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11

DeMille, Desiree, Bryan D. Badal, J. Brady Evans, Andrew D. Mathis, Joseph F. Anderson, and Julianne H. Grose. "PAS kinase is activated by direct SNF1-dependent phosphorylation and mediates inhibition of TORC1 through the phosphorylation and activation of Pbp1." Molecular Biology of the Cell 26, no. 3 (February 2015): 569–82. http://dx.doi.org/10.1091/mbc.e14-06-1088.

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We describe the interplay between three sensory protein kinases in yeast: AMP-regulated kinase (AMPK, or SNF1 in yeast), PAS kinase 1 (Psk1 in yeast), and the target of rapamycin complex 1 (TORC1). This signaling cascade occurs through the SNF1-dependent phosphorylation and activation of Psk1, which phosphorylates and activates poly(A)- binding protein binding protein 1 (Pbp1), which then inhibits TORC1 through sequestration at stress granules. The SNF1-dependent phosphorylation of Psk1 appears to be direct, in that Snf1 is necessary and sufficient for Psk1 activation by alternate carbon sources, is required for altered Psk1 protein mobility, is able to phosphorylate Psk1 in vitro, and binds Psk1 via its substrate-targeting subunit Gal83. Evidence for the direct phosphorylation and activation of Pbp1 by Psk1 is also provided by in vitro and in vivo kinase assays, including the reduction of Pbp1 localization at distinct cytoplasmic foci and subsequent rescue of TORC1 inhibition in PAS kinase–deficient yeast. In support of this signaling cascade, Snf1-deficient cells display increased TORC1 activity, whereas cells containing hyperactive Snf1 display a PAS kinase–dependent decrease in TORC1 activity. This interplay between yeast SNF1, Psk1, and TORC1 allows for proper glucose allocation during nutrient depletion, reducing cell growth and proliferation when energy is low.

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12

Berg, Tracey, Neville Firth, Sumalee Apisiridej, Anusha Hettiaratchi, Amornrut Leelaporn, and Ronald A. Skurray. "Complete Nucleotide Sequence of pSK41: Evolution of Staphylococcal Conjugative Multiresistance Plasmids." Journal of Bacteriology 180, no. 17 (September 1, 1998): 4350–59. http://dx.doi.org/10.1128/jb.180.17.4350-4359.1998.

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ABSTRACT The 46.4-kb nucleotide sequence of pSK41, a prototypical multiresistance plasmid from Staphylococcus aureus, has been determined, representing the first completely sequenced conjugative plasmid from a gram-positive organism. Analysis of the sequence has enabled the identification of the probable replication, maintenance, and transfer functions of the plasmid and has provided insights into the evolution of a clinically significant group of plasmids. The basis of deletions commonly associated with pSK41 family plasmids has been investigated, as has the observed insertion site specificity of Tn552-like β-lactamase transposons within them. Several of the resistance determinants carried by pSK41-like plasmids were found to be located on up to four smaller cointegrated plasmids. pSK41 and related plasmids appear to represent a consolidation of antimicrobial resistance functions, collected by a preexisting conjugative plasmid via transposon insertion and IS257-mediated cointegrative capture of other plasmids.

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13

Tosh, Pritish K., Simon Agolory, Bethany L. Strong, Kerrie VerLee, Jennie Finks, Kayoko Hayakawa, Teena Chopra, et al. "Prevalence and Risk Factors Associated with Vancomycin-Resistant Staphylococcus aureus Precursor Organism Colonization among Patients with Chronic Lower-Extremity Wounds in Southeastern Michigan." Infection Control & Hospital Epidemiology 34, no. 9 (September 2013): 954–60. http://dx.doi.org/10.1086/671735.

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Background.Of the 13 US vancomycin-resistant Staphylococcus aureus (VRSA) cases, 8 were identified in southeastern Michigan, primarily in patients with chronic lower-extremity wounds. VRSA infections develop when the vanA gene from vancomycin-resistant enterococcus (VRE) transfers to S. aureus. Incl8-like plasmids in VRE and pSK41-like plasmids in S. aureus appear to be important precursors to this transfer.Objective.Identify the prevalence of VRSA precursor organisms.Design.Prospective cohort with embedded case-control study.Participants.Southeastern Michigan adults with chronic lower-extremity wounds.Methods.Adults presenting to 3 southeastern Michigan medical centers during the period February 15 through March 4, 2011, with chronic lower-extremity wounds had wound, nares, and perirectal swab specimens cultured for S. aureus and VRE, which were tested for pSK41-like and Incl8-like plasmids by polymerase chain reaction. We interviewed participants and reviewed clinical records. Risk factors for pSK41-positive S. aureus were assessed among all study participants (cohort analysis) and among only S. aureus-colonized participants (case-control analysis).Results.Of 179 participants with wound cultures, 26% were colonized with methicillin-susceptible S. aureus, 27% were colonized with methicillin-resistant S. aureus, and 4% were colonized with VRE, although only 17% consented to perirectal culture. Six participants (3%) had pSK41-positive S. aureus, and none had Incl8-positive VRE. Having chronic wounds for over 2 years was associated with pSK41-positive S. aureus colonization in both analyses.Conclusions.Colonization with VRSA precursor organisms was rare. Having long-standing chronic wounds was a risk factor for pSK41-positive S. aureus colonization. Additional investigation into the prevalence of VRSA precursors among a larger cohort of patients is warranted.

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14

Albrecht, Valerie S., Marcus J. Zervos, Keith S. Kaye, Pritish K. Tosh, Samia Arshad, Kayoko Hayakawa, Alexander J. Kallen, Linda K. McDougal, Brandi M. Limbago, and Alice Y. Guh. "Prevalence of and Risk Factors for Vancomycin-Resistant Staphylococcus aureus Precursor Organisms in Southeastern Michigan." Infection Control & Hospital Epidemiology 35, no. 12 (December 2014): 1531–34. http://dx.doi.org/10.1086/593316.

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We assessed for vancomycin-resistantStaphylococcus aureus(VRSA) precursor organisms in southeastern Michigan, an area known to have VRSA. The prevalence was 2.5% (pSK41-positive methicillin-resistantS. aureus, 2009–2011) and 1.5% (Inc18-positive vancomycin-resistantEnterococcus, 2006–2013); Inc18 prevalence significantly decreased after 2009 (3.7% to 0.82%). Risk factors for pSK41 included intravenous vancomycin exposure.Infect Control Hosp Epidemiol2014;35(12):1531–1534

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15

Albrecht, Valerie S., Marcus J. Zervos, Keith S. Kaye, Pritish K. Tosh, Samia Arshad, Kayoko Hayakawa, Alexander J. Kallen, Linda K. McDougal, Brandi M. Limbago, and Alice Y. Guh. "Prevalence of and Risk Factors for Vancomycin-Resistant Staphylococcus aureus Precursor Organisms in Southeastern Michigan." Infection Control & Hospital Epidemiology 35, no. 12 (December 2014): 1531–34. http://dx.doi.org/10.1086/678605.

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We assessed for vancomycin-resistant Staphylococcus aureus (VRSA) precursor organisms in southeastern Michigan, an area known to have VRSA. The prevalence was 2.5% (pSK41-positive methicillin-resistant S. aureus, 2009–2011) and 1.5% (Inc18-positive vancomycin-resistant Enterococcus, 2006–2013); Inc18 prevalence significantly decreased after 2009 (3.7% to 0.82%). Risk factors for pSK41 included intravenous vancomycin exposure.Infect Control Hosp Epidemiol 2014;35(12):1531–1534

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16

Yin, Hang, Danni Yin, Mingzhi Zhang, Zhiqiang Gao, Muzhapaer Tuluhong, Xiaoming Li, Jikai Li, Bing Li, and Guowen Cui. "Validation of Appropriate Reference Genes for qRT–PCR Normalization in Oat (Avena sativa L.) under UV-B and High-Light Stresses." International Journal of Molecular Sciences 23, no. 19 (September 23, 2022): 11187. http://dx.doi.org/10.3390/ijms231911187.

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Oat is a food and forage crop species widely cultivated worldwide, and it is also an important forage grass in plateau regions of China, where there is a high level of ultraviolet radiation and sunlight. Screening suitable reference genes for oat under UV-B and high-light stresses is a prerequisite for ensuring the accuracy of real-time quantitative PCR (qRT–PCR) data used in plant adaptation research. In this study, eight candidate reference genes (sulfite oxidase, SUOX; victorin binding protein, VBP; actin-encoding, Actin1; protein PSK SIMULATOR 1-like, PSKS1; TATA-binding protein 2-like, TBP2; ubiquitin-conjugating enzyme E2, UBC2; elongation factor 1-alpha, EF1-α; glyceraldehyde-3-phosphate dehydrogenase 1, GAPDH1;) were selected based on previous studies and our oat transcriptome data. The expression stability of these reference genes in oat roots, stems, and leaves under UV-B and high-light stresses was first calculated using three frequently used statistical software (geNorm, NormFinder, and BestKeeper), and then the comprehensive stability of these genes was evaluated using RefFinder. The results showed that the most stably expressed reference genes in the roots, stems, and leaves of oat under UV-B stress were EF1-α, TBP2, and PSKS1, respectively; the most stably expressed reference genes in the roots, stems, and leaves under high-light stress were PSKS1, UBC2, and PSKS1, respectively. PSKS1 was the most stably expressed reference gene in all the samples. The reliability of the selected reference genes was further validated by analysis of the expression of the phenylalanine ammonia-lyase (PAL) gene. This study highlights reference genes for accurate quantitative analysis of gene expression in different tissues of oat under UV-B and high-light stresses.

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17

Kong, Hye Suk, Daniel P. Roberts, Cheryl D. Patterson, Sarah A. Kuehne, Stephan Heeb, Dilip K. Lakshman, and John Lydon. "Effect of Overexpressing rsmA from Pseudomonas aeruginosa on Virulence of Select Phytotoxin-Producing Strains of P. syringae." Phytopathology® 102, no. 6 (June 2012): 575–87. http://dx.doi.org/10.1094/phyto-09-11-0267.

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The GacS/GacA two-component system functions mechanistically in conjunction with global post-transcriptional regulators of the RsmA family to allow pseudomonads and other bacteria to adapt to changing environmental stimuli. Analysis of this Gac/Rsm signal transduction pathway in phytotoxin-producing pathovars of Pseudmonas syringae is incomplete, particularly with regard to rsmA. Our approach in studying it was to overexpress rsmA in P. syringae strains through introduction of pSK61, a plasmid constitutively expressing this gene. Disease and colonization of plant leaf tissue were consistently diminished in all P. syringae strains tested (pv. phaseolicola NPS3121, pv. syringae B728a, and BR2R) when harboring pSK61 relative to these isolates harboring the empty vector pME6031. Phaseolotoxin, syringomycin, and tabtoxin were not produced in any of these strains when transformed with pSK61. Production of protease and pyoverdin as well as swarming were also diminished in all of these strains when harboring pSK61. In contrast, alginate production, biofilm formation, and the hypersensitive response were diminished in some but not all of these isolates under the same growth conditions. These results indicate that rsmA is consistently important in the overarching phenotypes disease and endophtyic colonization but that its role varies with pathovar in certain underpinning phenotypes in the phytotoxin-producing strains of P. syringae.

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18

Wang, Wen-Ying, Han-Feng Ding, Guang-Xian Li, Ming-Song Jiang, Run-Fang Li, Xu Liu, Yu Zhang, and Fang-Yin Yao. "Delimitation of thePSH1(t) gene for rice purple leaf sheath to a 23.5 kb DNA fragment." Genome 52, no. 3 (March 2009): 268–74. http://dx.doi.org/10.1139/g08-121.

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Leaf sheath color plays an important role as a marker for rice genetic improvement. A recombinant inbred line (RIL) population consisting of 220 individuals was developed from a cross between an Oryza sativa subsp. indica variety, IRBB60, and an Oryza sativa subsp. japonica variery, 9407. Within the RIL population, a line, RI51, was found to have purple leaf sheath (PSH). To map the gene governing PSH, RI51 was crossed with 9407 green leaf sheath (GSH) to develop an F2segregating population. The distribution of F2plants with PSH and GSH fitted a segregation ratio of 3:1, indicating that the PSH was controlled by a major dominant gene. The gene locus for PSH, tentatively designated as PSH1(t), was identified by surveying two bulks made of the respective 40 individuals with PSH and GSH with SSR markers covering the entire rice genome. The survey indicated that the PSH1(t) region was located on chromosome 1. Further confirmation was made using a large random sample of 360 individuals from the same F2population and the PSH1(t) locus was then mapped on chromosome 1 between SSR markers RM3475 and RM7202 with genetic distances of 2.0 and 1.1 cM, respectively. For fine mapping of PSH1(t), a large F2:3segregating population with 3300 individuals from the seven heterozygous F2plants in the RM3475–RM7202 region was constructed. Analysis of recombinants in the PSH1(t) region anchored the gene locus to an interval of 23.5 kb flanked by the left marker L03 and the right marker L05. Sequence analysis of this fragment predicted six open reading frames encoding a putative trans-sialidase, a putative Plastidic ATP/ADP-transporter, and four unknown proteins. The detailed genetic and physical maps of the PSH1(t) locus will be very useful in molecular cloning of the PSH1(t) gene.

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19

McDougal, Linda K., Gregory E. Fosheim, Ainsley Nicholson, Sandra N. Bulens, Brandi M. Limbago, Julia E. S. Shearer, Anne O. Summers, and Jean B. Patel. "Emergence of Resistance among USA300 Methicillin-Resistant Staphylococcus aureus Isolates Causing Invasive Disease in the United States." Antimicrobial Agents and Chemotherapy 54, no. 9 (June 28, 2010): 3804–11. http://dx.doi.org/10.1128/aac.00351-10.

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ABSTRACT USA300 methicillin-resistant Staphylococcus aureus (MRSA) isolates are usually resistant only to oxacillin, erythromycin, and, increasingly, levofloxacin. Of these, oxacillin and levofloxacin resistances are chromosomally encoded. Plasmid-mediated clindamycin, mupirocin, and/or tetracycline resistance has been observed among USA300 isolates, but these descriptions were limited to specific patient populations or isolated occurrences. We examined the antimicrobial susceptibilities of invasive MRSA isolates from a national surveillance population in order to identify USA300 isolates with unusual, possibly emerging, plasmid-mediated antimicrobial resistance. DNA from these isolates was assayed for the presence of resistance determinants and the presence of a pSK41-like conjugative plasmid. Of 823 USA300 isolates, 72 (9%) were tetracycline resistant; 69 of these were doxycycline susceptible and tet K positive, and 3 were doxycycline resistant and tet M positive. Fifty-one (6.2%) isolates were clindamycin resistant and erm C positive; 22 (2.7%) isolates were high-level mupirocin resistant (mup A positive); 5 (0.6%) isolates were trimethoprim-sulfamethoxazole (TMP-SMZ) resistant, of which 4 were dfr A positive; and 7 (0.9%) isolates were gentamicin resistant and aac 6′-aph 2″ positive. Isolates with pSK41-like plasmids (n = 24) were positive for mup A (n = 19), dfr A (n = 6), aac 6′-aph 2″ (n = 6), tet M (n = 2), and erm C (n = 8); 20 pSK41-positive isolates were positive for two or more resistance genes. Conjugative transfer of resistance was demonstrated between four gentamicin- and mupirocin-resistant and three gentamicin- and TMP-SMZ-resistant USA300 isolates; transconjugants harbored a single pSK41-like plasmid, which was PCR positive for aac 6′-aph 2″ and either mup A and/or dfr A. USA300 and USA100 isolates from the same state with identical resistance profiles contained pSK41-like plasmids with indistinguishable restriction and Southern blot profiles, suggesting horizontal plasmid transfer between USA100 and USA300 isolates.

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20

Kaufmann, Christine, Nils Stührwohldt, and Margret Sauter. "Tyrosylprotein sulfotransferase-dependent and -independent regulation of root development and signaling by PSK LRR receptor kinases in Arabidopsis." Journal of Experimental Botany 72, no. 15 (May 24, 2021): 5508–21. http://dx.doi.org/10.1093/jxb/erab233.

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Abstract Tyrosine-sulfated peptides are key regulators of plant growth and development. The disulfated pentapeptide phytosulfokine (PSK) mediates growth via leucine-rich repeat receptor-like kinases, PSKR1 and PSKR2. PSK receptors (PSKRs) are part of a response module at the plasma membrane that mediates short-term growth responses, but downstream signaling of transcriptional regulation remains unexplored. In Arabidopsis, tyrosine sulfation is catalyzed by a single-copy gene (TPST; encoding tyrosylprotein sulfotransferase). We performed a microarray-based transcriptome analysis in the tpst-1 mutant background that lacks sulfated peptides to identify PSK-regulated genes and genes that are regulated by other sulfated peptides. Of the 169 PSK-regulated genes, several had functions in root growth and development, in agreement with shorter roots and a higher lateral root density in tpst-1. Further, tpst-1 roots developed higher numbers of root hairs, and PSK induced expression of WEREWOLF (WER), its paralog MYB DOMAIN PROTEIN 23 (MYB23), and At1g66800 that maintain non-hair cell fate. The tpst-1 pskr1-3 pskr2-1 mutant showed even shorter roots, and higher lateral root and root hair density than tpst-1, revealing unexpected synergistic effects of ligand and PSKR deficiencies. While residual activities may exist, overexpression of PSKR1 in the tpst-1 background induced root growth, suggesting that PSKR1 may be active in the absence of sulfated ligands.

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21

Rayhan al-Biruni, Abu. "Kitab Patanjali (Introdiction)." Islam in the modern world 17, no. 2 (July 23, 2021): 83–88. http://dx.doi.org/10.22311/2074-1529-2021-17-2-83-88.

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22

Zhukov, Vladimir, Simona Radutoiu, Lene H. Madsen, Tamara Rychagova, Evgenia Ovchinnikova, Alex Borisov, Igor Tikhonovich, and Jens Stougaard. "The Pea Sym37 Receptor Kinase Gene Controls Infection-Thread Initiation and Nodule Development." Molecular Plant-Microbe Interactions® 21, no. 12 (December 2008): 1600–1608. http://dx.doi.org/10.1094/mpmi-21-12-1600.

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Phenotypic characterization of pea symbiotic mutants has provided a detailed description of the symbiosis with Rhizobium leguminosarum bv. viciae strains. We show here that two allelic non-nodulating pea mutants, RisNod4 and K24, are affected in the PsSym37 gene, encoding a LysM receptor kinase similar to Lotus japonicus NFR1 and Medicago truncatula LYK3. Phenotypic analysis of RisNod4 and K24 suggests a role for the SYM37 in regulation of infection-thread initiation and nodule development from cortical-cell division foci. We show that RisNod4 plants carrying an L to F substitution in the LysM1 domain display a restrictive symbiotic phenotype comparable to the PsSym2A lines that distinguish ‘European’ and ‘Middle East’ Rhizobium leguminosarum bv. viciae strains. RisNod4 mutants develop nodules only in the presence of a ‘Middle East’ Rhizobium strain producing O-acetylated Nod factors indicating the SYM37 involvement in Nod-factor recognition. Along with the PsSym37, a homologous LysM receptor kinase gene, PsK1, was isolated and characterized. We show that PsK1 and PsSym37 are genetically linked to each other and to the PsSym2 locus. Allelic complementation analyses and sequencing of the extracellular regions of PsSym37 and PsK1 in several ‘European’ and ‘Afghan’ pea cultivars point towards PsK1 as possible candidate for the elusive PsSym2 gene.

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23

Ohkuni, Kentaro, Yoshimitsu Takahashi, Alyona Fulp, Josh Lawrimore, Wei-Chun Au, Nagesh Pasupala, Reuben Levy-Myers, et al. "SUMO-targeted ubiquitin ligase (STUbL) Slx5 regulates proteolysis of centromeric histone H3 variant Cse4 and prevents its mislocalization to euchromatin." Molecular Biology of the Cell 27, no. 9 (May 2016): 1500–1510. http://dx.doi.org/10.1091/mbc.e15-12-0827.

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Centromeric histone H3, CENP-ACse4, is essential for faithful chromosome segregation. Stringent regulation of cellular levels of CENP-ACse4 restricts its localization to centromeres. Mislocalization of CENP-ACse4 is associated with aneuploidy in yeast and flies and tumorigenesis in human cells; thus defining pathways that regulate CENP-A levels is critical for understanding how mislocalization of CENP-A contributes to aneuploidy in human cancers. Previous work in budding yeast shows that ubiquitination of overexpressed Cse4 by Psh1, an E3 ligase, partially contributes to proteolysis of Cse4. Here we provide the first evidence that Cse4 is sumoylated by E3 ligases Siz1 and Siz2 in vivo and in vitro. Ubiquitination of Cse4 by the small ubiquitin-related modifier (SUMO)-targeted ubiquitin ligase (STUbL) Slx5 plays a critical role in proteolysis of Cse4 and prevents mislocalization of Cse4 to euchromatin under normal physiological conditions. Accumulation of sumoylated Cse4 species and increased stability of Cse4 in slx5∆ strains suggest that sumoylation precedes ubiquitin-mediated proteolysis of Cse4. Slx5-mediated Cse4 proteolysis is independent of Psh1, since slx5∆ psh1∆ strains exhibit higher levels of Cse4 stability and mislocalization than either slx5∆ or psh1∆ strains. Our results demonstrate a role for Slx5 in ubiquitin-mediated proteolysis of Cse4 to prevent its mislocalization and maintain genome stability.

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24

Muleya, Victor, Claudius Marondedze, Janet I. Wheeler, Ludivine Thomas, Yee-Fong Mok, Michael D. W. Griffin, David T. Manallack, et al. "Phosphorylation of the dimeric cytoplasmic domain of the phytosulfokine receptor, PSKR1." Biochemical Journal 473, no. 19 (September 27, 2016): 3081–98. http://dx.doi.org/10.1042/bcj20160593.

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Phytosulfokines (PSKs) are plant peptide hormones that co-regulate plant growth, differentiation and defense responses. PSKs signal through a plasma membrane localized leucine-rich repeat receptor-like kinase (phytosulfokine receptor 1, PSKR1) that also contains a functional cytosolic guanylate cyclase with its cyclase catalytic center embedded within the kinase domain. To functionally characterize this novel type of overlapping dual catalytic function, we investigated the phosphorylation of PSKR1 in vitro. Tandem mass spectrometry of the cytoplasmic domain of PSKR1 (PSKR1cd) revealed at least 11 phosphorylation sites (8 serines, 2 threonines and 1 tyrosine) within the PSKR1cd. Phosphomimetic mutations of three serine residues (Ser686, Ser696 and Ser698) in tandem at the juxta-membrane position resulted in enhanced kinase activity in the on-mutant that was suppressed in the off-mutant, but both mutations reduced guanylate cyclase activity. Both the on and off phosphomimetic mutations of the phosphotyrosine (Tyr888) residue in the activation loop suppressed kinase activity, while neither mutation affected guanylate cyclase activity. Size exclusion and analytical ultracentrifugation analysis of the PSKR1cd suggest that it is reversibly dimeric in solution, which was further confirmed by biflourescence complementation. Taken together, these data suggest that in this novel type of receptor domain architecture, specific phosphorylation and dimerization are possibly essential mechanisms for ligand-mediated catalysis and signaling.

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25

Rosaef, Jemimma Pamelasari, Dwi Utari Rahmiati, and Budi Sujatmiko. "Korelasi Prestasi Akademik dengan Nilai Keterikatan Interaksi Manusia-Hewan Menggunakan Pet Attachment and Life Impact Scale." Indonesia Medicus Veterinus 9, no. 3 (May 31, 2020): 401–16. http://dx.doi.org/10.19087/imv.2020.9.3.401.

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Interaksi antara manusia dengan hewan telah terjadi selama puluhan ribu tahun yang lalu. Interaksi manusia dengan hewan memiliki berbagai efek yang positif terhadap manusia, terutama dalam aspek kognitif dan pendidikan. Penelitian ini bertujuan untuk mengetahui gambaran interaksi manusia dan hewan, hubungan, serta kuatnya hubungan prestasi akademik mahasiswa kedokteran hewan dengan nilai keterikatan interaksi manusia dan hewan menggunakan instrument Pet Attachment and Life Impact Scale (PALS). Subjek dalam penelitian merupakan mahasiswa Program Studi Kedokteran Hewan (PSKH) Universitas Padjadjaran yang memiliki hewan peliharaan dan tinggal bersama atau pernah tinggal bersama hewan peliharaan. Metode penelitian menggunakan teknik survei dengan instrument kuesioner PALS. Data yang diperoleh dianalisis menggunakan uji korelasi Spearman. Berdasarkan penelitian didapatkan hasil bahwa terdapat Korelasi positif antara prestasi akademik mahasiswa PSKH Unpad dengan nilai keterikatan interaksi manusia dan hewan dengan kekuatan hubungan sebesar r = 0,26 dan p-value = < 0,001. Kuatnya hubungan tersebut menunjukkan bahwa adanya interaksi manusia dan hewan dapat berpengaruh terhadap peningkatan prestasi akademik mahasiswa PSKH Unpad.

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26

Simpson, Alice E., Ronald A. Skurray, and Neville Firth. "A Single Gene on the Staphylococcal Multiresistance Plasmid pSK1 Encodes a Novel Partitioning System." Journal of Bacteriology 185, no. 7 (April 1, 2003): 2143–52. http://dx.doi.org/10.1128/jb.185.7.2143-2152.2003.

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ABSTRACT The orf245 gene is located immediately upstream of, and divergently transcribed from, the replication initiation gene, rep, of the Staphylococcus aureus multiresistance plasmid pSK1, and related genes have been found in association with a range of evolutionarily distinct replication genes on plasmids from various gram-positive genera. orf245 has been shown previously to extend the segregational stability of a pSK1 minireplicon. Here we describe an investigation into the basis of orf245-mediated stabilization. orf245 was not found to influence transcription of pSK1 rep, indicating that it is not directly involved in plasmid replication. This was confirmed by demonstrating that orf245 is able to enhance the segregational stability of heterologous theta- and rolling-circle-replicating replicons, suggesting that it encodes a plasmid maintenance function. Evidence inconsistent with postsegregational killing and multimer resolution mechanisms was obtained; however, the intergenic region upstream of orf245 was found to mediate orf245-dependent incompatibility, as would be expected if it encodes a cis-acting centromere-like site. Taken together, these findings implicate active partitioning as the probable basis of the activity of orf245, which is therefore redesignated par. Since it is unrelated to any gene known to play a role in plasmid segregation, it seems likely that pSK1 par potentially represents the prototype of a novel class of active partitioning systems that are distinguished by their capacity to enhance plasmid segregational stability via a single protein-encoding gene.

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Mishra, Prashant K., Jiasheng Guo, Lauren E. Dittman, Julian Haase, Elaine Yeh, Kerry Bloom, and Munira A. Basrai. "Pat1 protects centromere-specific histone H3 variant Cse4 from Psh1-mediated ubiquitination." Molecular Biology of the Cell 26, no. 11 (June 2015): 2067–79. http://dx.doi.org/10.1091/mbc.e14-08-1335.

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Evolutionarily conserved histone H3 variant Cse4 and its homologues are essential components of specialized centromere ( CEN)-specific nucleosomes and serve as an epigenetic mark for CEN identity and propagation. Cse4 is a critical determinant for the structure and function of the kinetochore and is required to ensure faithful chromosome segregation. The kinetochore protein Pat1 regulates the levels and spatial distribution of Cse4 at centromeres. Deletion of PAT1 results in altered structure of CEN chromatin and chromosome segregation errors. In this study, we show that Pat1 protects CEN-associated Cse4 from ubiquitination in order to maintain proper structure and function of the kinetochore in budding yeast. PAT1-deletion strains exhibit increased ubiquitination of Cse4 and faster turnover of Cse4 at kinetochores. Psh1, a Cse4-specific E3-ubiquitin ligase, interacts with Pat1 in vivo and contributes to the increased ubiquitination of Cse4 in pat1∆ strains. Consistent with a role of Psh1 in ubiquitination of Cse4, transient induction of PSH1 in a wild-type strain resulted in phenotypes similar to a pat1∆ strain, including a reduction in CEN-associated Cse4, increased Cse4 ubiquitination, defects in spatial distribution of Cse4 at kinetochores, and altered structure of CEN chromatin. Pat1 interacts with Scm3 and is required for its maintenance at kinetochores. In conclusion, our studies provide novel insights into mechanisms by which Pat1 affects the structure of CEN chromatin and protects Cse4 from Psh1-mediated ubiquitination for faithful chromosome segregation.

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28

Zheng, Yan, Mjomba Fredrick Mwamburi, Huaqing Liu, and Feng Wang. "Loss of Function of OsARG Resulted in Pepper-Shaped Husk in Indica Rice." Life 11, no. 6 (June 3, 2021): 523. http://dx.doi.org/10.3390/life11060523.

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Grain shape is one of the most important and complex traits determining the grain yield in rice. In this study, we discovered two rice mutants with defective shape spikelets, designated as psh1-1/2 (pepper-shaped husk 1-1/2), which were both isolated from the tissue-culture-regenerated plants of indica cultivar Minghui 86. The two mutants showed the same mutant phenotypes, containing pepper-shaped spikelets; shorter, smaller and compact panicles; very low seed-setting rate; high percentage of split grains; and lower grain width. Genetic analysis indicated that the mutant phenotypes were controlled by a recessive gene. Gene mapping indicated that the target gene PSH1 was located on the short arm of chromosome 4. Sequencing analysis revealed that the two mutants each had a different nonsense mutation in OsARG, confirming that the target gene is OsARG. Compared with the previously reported OsARG mutant nglf-1, psh1-1/2 possessed some distinct mutant phenotypes, probably because of the influence of different genetic background, suggesting that OsARG may function differently under different genetic backgrounds.

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29

Liu, Michael A., Stephen M. Kwong, Slade O. Jensen, Anthony J. Brzoska, and Neville Firth. "Biology of the staphylococcal conjugative multiresistance plasmid pSK41." Plasmid 70, no. 1 (July 2013): 42–51. http://dx.doi.org/10.1016/j.plasmid.2013.02.001.

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30

Kwong, Stephen M., Ronald A. Skurray, and Neville Firth. "Replication Control of Staphylococcal Multiresistance Plasmid pSK41: an Antisense RNA Mediates Dual-Level Regulation of Rep Expression." Journal of Bacteriology 188, no. 12 (June 15, 2006): 4404–12. http://dx.doi.org/10.1128/jb.00030-06.

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ABSTRACT Replication of staphylococcal multiresistance plasmid pSK41 is negatively regulated by the antisense transcript RNAI. pSK41 minireplicons bearing rnaI promoter (P rnaI ) mutations exhibited dramatic increases in copy number, approximately 40-fold higher than the copy number for the wild-type replicon. The effects of RNAI mutations on expression of the replication initiator protein (Rep) were evaluated using transcriptional and translational fusions between the rep control region and the cat reporter gene. The results suggested that when P rnaI is disrupted, the amount of rep mRNA increases and it becomes derepressed for translation. These effects were reversed when RNAI was provided in trans, demonstrating that it is responsible for significant negative regulation at two levels, with the greatest repression exerted on rep translation initiation. Mutagenesis provided no evidence for RNAI-mediated transcriptional attenuation as a basis for the observed reduction in rep message associated with expression of RNAI. However, RNA secondary-structure predictions and supporting mutagenesis data suggest a novel mechanism for RNAI-mediated repression of rep translation initiation, where RNAI binding promotes a steric transition in the rep mRNA leader to an alternative thermodynamically stable stem-loop structure that sequesters the rep translation initiation region, thereby preventing translation.

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31

Belov, Vladimir N., and Tigran G. Tumanian. "Gerhard Oberhammer: indologist and philosopher. Ed. Ruzana V. Pskhu." Voprosy Filosofii, no. 10 (2020): 219–21. http://dx.doi.org/10.21146/0042-8744-2020-10-219-221.

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32

Mosher, Stephen, and Birgit Kemmerling. "PSKR1 and PSY1R-mediated regulation of plant defense responses." Plant Signaling & Behavior 8, no. 5 (May 2013): e24119. http://dx.doi.org/10.4161/psb.24119.

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33

Eisenstatt, Jessica R., Lars Boeckmann, Wei-Chun Au, Valerie Garcia, Levi Bursch, Josefina Ocampo, Michael Costanzo, et al. "Dbf4-Dependent Kinase (DDK)-Mediated Proteolysis of CENP-A Prevents Mislocalization of CENP-A in Saccharomyces cerevisiae." G3: Genes|Genomes|Genetics 10, no. 6 (April 15, 2020): 2057–68. http://dx.doi.org/10.1534/g3.120.401131.

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The evolutionarily conserved centromeric histone H3 variant (Cse4 in budding yeast, CENP-A in humans) is essential for faithful chromosome segregation. Mislocalization of CENP-A to non-centromeric chromatin contributes to chromosomal instability (CIN) in yeast, fly, and human cells and CENP-A is highly expressed and mislocalized in cancers. Defining mechanisms that prevent mislocalization of CENP-A is an area of active investigation. Ubiquitin-mediated proteolysis of overexpressed Cse4 (GALCSE4) by E3 ubiquitin ligases such as Psh1 prevents mislocalization of Cse4, and psh1Δ strains display synthetic dosage lethality (SDL) with GALCSE4. We previously performed a genome-wide screen and identified five alleles of CDC7 and DBF4 that encode the Dbf4-dependent kinase (DDK) complex, which regulates DNA replication initiation, among the top twelve hits that displayed SDL with GALCSE4. We determined that cdc7-7 strains exhibit defects in ubiquitin-mediated proteolysis of Cse4 and show mislocalization of Cse4. Mutation of MCM5 (mcm5-bob1) bypasses the requirement of Cdc7 for replication initiation and rescues replication defects in a cdc7-7 strain. We determined that mcm5-bob1 does not rescue the SDL and defects in proteolysis of GALCSE4 in a cdc7-7 strain, suggesting a DNA replication-independent role for Cdc7 in Cse4 proteolysis. The SDL phenotype, defects in ubiquitin-mediated proteolysis, and the mislocalization pattern of Cse4 in a cdc7-7 psh1Δ strain were similar to that of cdc7-7 and psh1Δ strains, suggesting that Cdc7 regulates Cse4 in a pathway that overlaps with Psh1. Our results define a DNA replication initiation-independent role of DDK as a regulator of Psh1-mediated proteolysis of Cse4 to prevent mislocalization of Cse4.

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34

Freihat, Lubna, Victor Muleya, David T. Manallack, Janet I. Wheeler, and Helen R. Irving. "Comparison of moonlighting guanylate cyclases: roles in signal direction?" Biochemical Society Transactions 42, no. 6 (November 17, 2014): 1773–79. http://dx.doi.org/10.1042/bst20140223.

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Over 30 receptor-like kinases contain a guanylate cyclase (GC) catalytic centre embedded within the C-terminal region of their kinase domain in the model plant Arabidopsis. A number of the kinase GCs contain both functional kinase and GC activity in vitro and the natural ligands of these receptors stimulate increases in cGMP within isolated protoplasts. The GC activity could be described as a minor or moonlighting activity. We have also identified mammalian proteins that contain the novel GC centre embedded within kinase domains. One example is the interleukin 1 receptor-associated kinase 3 (IRAK3). We compare the GC functionality of the mammalian protein IRAK3 with the cytoplasmic domain of the plant prototype molecule, the phytosulfokine receptor 1 (PSKR1). We have developed homology models of these molecules and have undertaken in vitro experiments to compare their functionality and structural features. Recombinant IRAK3 produces cGMP at levels comparable to those produced by PSKR1, suggesting that IRAK3 contains GC activity. Our findings raise the possibility that kinase-GCs may switch between downstream kinase-mediated or cGMP-mediated signalling cascades to elicit desired outputs to particular stimuli. The challenge now lies in understanding the interaction between the GC and kinase domains and how these molecules utilize their dual functionality within cells.

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Li, Ronghui, Maggie R. Knox, Anne Edwards, Bridget Hogg, T. H. Noel Ellis, Gehong Wei, and J. Allan Downie. "Natural Variation in Host-Specific Nodulation of Pea Is Associated with a Haplotype of the SYM37 LysM-Type Receptor-Like Kinase." Molecular Plant-Microbe Interactions® 24, no. 11 (November 2011): 1396–403. http://dx.doi.org/10.1094/mpmi-01-11-0004.

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Rhizobium leguminosarum bv. viciae, which nodulates pea and vetch, makes a mixture of secreted nodulation signals (Nod factors) carrying either a C18:4 or a C18:1 N-linked acyl chain. Mutation of nodE blocks the formation of the C18:4 acyl chain, and nodE mutants, which produce only C18:1-containing Nod factors, are less efficient at nodulating pea. However, there is significant natural variation in the levels of nodulation of different pea cultivars by a nodE mutant of R. leguminosarum bv. viciae. Using recombinant inbred lines from two pea cultivars, one which nodulated relatively well and one very poorly by the nodE mutant, we mapped the nodE-dependent nodulation phenotype to a locus on pea linkage group I. This was close to Sym37 and PsK1, predicted to encode LysM-domain Nod-factor receptor-like proteins; the Sym2 locus that confers Nod-factor-specific nodulation is also in this region. We confirmed the map location using an introgression line carrying this region. Our data indicate that the nodE-dependent nodulation is not determined by the Sym2 locus. We identified several pea lines that are nodulated very poorly by the R. leguminosarum bv. viciae nodE mutant, sequenced the DNA of the predicted LysM-receptor domains of Sym37 and PsK1, and compared the sequences with those derived from pea cultivars that were relatively well nodulated by the nodE mutant. This revealed that one haplotype (encoding six conserved polymorphisms) of Sym37 is associated with very poor nodulation by the nodE mutant. There was no such correlation with polymorphisms at the PsK1 locus. We conclude that the natural variation in nodE-dependent nodulation in pea is most probably determined by the Sym37 haplotype.

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36

Hewawasam, Geetha S., and Jennifer L. Gerton. "Cse4 gets a kiss-of-death from Psh1." Cell Cycle 10, no. 4 (February 15, 2011): 566–67. http://dx.doi.org/10.4161/cc.10.4.14770.

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Reuther, Jens, Wolfgang Wohlleben, and Günther Muth. "Modular architecture of the conjugative plasmid pSVH1 from Streptomyces venezuelae." Plasmid 55, no. 3 (May 2006): 201–9. http://dx.doi.org/10.1016/j.plasmid.2005.11.007.

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38

Kaufmann, Christine, Michael Motzkus, and Margret Sauter. "Phosphorylation of the phytosulfokine peptide receptor PSKR1 controls receptor activity." Journal of Experimental Botany 68, no. 7 (February 23, 2017): 1411–23. http://dx.doi.org/10.1093/jxb/erx030.

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39

Lee, Dae-Ryung, Keun-Seong Park, and Ki-Mon Kim. "A study on the implementation of digital fisheries information network using PSK31 on MH/HF radio Band." Journal of the Korean Institute of Information and Communication Engineering 14, no. 6 (June 30, 2010): 1365–74. http://dx.doi.org/10.6109/jkiice.2010.14.6.1365.

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40

DeMille, Desiree, Benjamin T. Bikman, Andrew D. Mathis, John T. Prince, Jordan T. Mackay, Steven W. Sowa, Tacie D. Hall, and Julianne H. Grose. "A comprehensive protein–protein interactome for yeast PAS kinase 1 reveals direct inhibition of respiration through the phosphorylation of Cbf1." Molecular Biology of the Cell 25, no. 14 (July 15, 2014): 2199–215. http://dx.doi.org/10.1091/mbc.e13-10-0631.

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Per-Arnt-Sim (PAS) kinase is a sensory protein kinase required for glucose homeostasis in yeast, mice, and humans, yet little is known about the molecular mechanisms of its function. Using both yeast two-hybrid and copurification approaches, we identified the protein–protein interactome for yeast PAS kinase 1 (Psk1), revealing 93 novel putative protein binding partners. Several of the Psk1 binding partners expand the role of PAS kinase in glucose homeostasis, including new pathways involved in mitochondrial metabolism. In addition, the interactome suggests novel roles for PAS kinase in cell growth (gene/protein expression, replication/cell division, and protein modification and degradation), vacuole function, and stress tolerance. In vitro kinase studies using a subset of 25 of these binding partners identified Mot3, Zds1, Utr1, and Cbf1 as substrates. Further evidence is provided for the in vivo phosphorylation of Cbf1 at T211/T212 and for the subsequent inhibition of respiration. This respiratory role of PAS kinase is consistent with the reported hypermetabolism of PAS kinase–deficient mice, identifying a possible molecular mechanism and solidifying the evolutionary importance of PAS kinase in the regulation of glucose homeostasis.

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41

Jensen, Slade O., Sumalee Apisiridej, Stephen M. Kwong, Yee Hwa Yang, Ronald A. Skurray, and Neville Firth. "Analysis of the prototypical Staphylococcus aureus multiresistance plasmid pSK1." Plasmid 64, no. 3 (November 2010): 135–42. http://dx.doi.org/10.1016/j.plasmid.2010.06.001.

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42

Guo, Peng, Qiuxiang Cheng, Pengfei Xie, Yun Fan, Weihong Jiang, and Zhongjun Qin. "Characterization of the multiple CRISPR loci on Streptomyces linear plasmid pSHK1." Acta Biochimica et Biophysica Sinica 43, no. 8 (June 24, 2011): 630–39. http://dx.doi.org/10.1093/abbs/gmr052.

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43

Liu, Michael A., Stephen M. Kwong, Cindy K. Pon, Ronald A. Skurray, and Neville Firth. "Genetic requirements for replication initiation of the staphylococcal multiresistance plasmid pSK41." Microbiology 158, no. 6 (June 1, 2012): 1456–67. http://dx.doi.org/10.1099/mic.0.057620-0.

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44

Popp, David, Weijun Xu, Akihiro Narita, Anthony J. Brzoska, Ronald A. Skurray, Neville Firth, Umesh Goshdastider, Yuichiro Maéda, Robert C. Robinson, and Maria A. Schumacher. "Structure and Filament Dynamics of the pSK41 Actin-like ParM Protein." Journal of Biological Chemistry 285, no. 13 (January 27, 2010): 10130–40. http://dx.doi.org/10.1074/jbc.m109.071613.

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45

Popp, David, Weijun Xu, Akihiro Narita, Anthony J. Brzoska, Ronald A. Skurray, Neville Firth, Umesh Ghoshdastider, Yuichiro Maéda, Robert C. Robinson, and Maria A. Schumacher. "Structure and filament dynamics of the pSK41 actin-like ParM protein." Journal of Biological Chemistry 285, no. 23 (May 28, 2010): 18122.5–18122. http://dx.doi.org/10.1074/jbc.a109.071613.

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46

Firth, Neville, Karyn P. Ridgway, Mary E. Byrne, Peter D. Fink, Luke Johnson, Ian T. Paulsen, and Ronald A. Skurray. "Analysis of a transfer region from the staphylococcal conjugative plasmid pSK41." Gene 136, no. 1-2 (December 1993): 13–25. http://dx.doi.org/10.1016/0378-1119(93)90442-6.

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47

Abate, Maedot, and Krystle McLaughlin. "Abstract 1447 Investigation of Conjugative Protein Orf90 from S. aureus pSK41." Journal of Biological Chemistry 300, no. 3 (March 2024): 106900. http://dx.doi.org/10.1016/j.jbc.2024.106900.

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48

Rauceo, Jason M., Jill R. Blankenship, Saranna Fanning, Jessica J. Hamaker, Jean-Sebastien Deneault, Frank J. Smith, Andre Nantel, and Aaron P. Mitchell. "Regulation of theCandida albicansCell Wall Damage Response by Transcription Factor Sko1 and PAS Kinase Psk1." Molecular Biology of the Cell 19, no. 7 (July 2008): 2741–51. http://dx.doi.org/10.1091/mbc.e08-02-0191.

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The environmental niche of each fungus places distinct functional demands on the cell wall. Hence cell wall regulatory pathways may be highly divergent. We have pursued this hypothesis through analysis of Candida albicans transcription factor mutants that are hypersensitive to caspofungin, an inhibitor of beta-1,3-glucan synthase. We report here that mutations in SKO1 cause this phenotype. C. albicans Sko1 undergoes Hog1-dependent phosphorylation after osmotic stress, like its Saccharomyces cerevisiae orthologues, thus arguing that this Hog1-Sko1 relationship is conserved. However, Sko1 has a distinct role in the response to cell wall inhibition because 1) sko1 mutants are much more sensitive to caspofungin than hog1 mutants; 2) Sko1 does not undergo detectable phosphorylation in response to caspofungin; 3) SKO1 transcript levels are induced by caspofungin in both wild-type and hog1 mutant strains; and 4) sko1 mutants are defective in expression of caspofungin-inducible genes that are not induced by osmotic stress. Upstream Sko1 regulators were identified from a panel of caspofungin-hypersensitive protein kinase–defective mutants. Our results show that protein kinase Psk1 is required for expression of SKO1 and of Sko1-dependent genes in response to caspofungin. Thus Psk1 and Sko1 lie in a newly described signal transduction pathway.

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49

Hewawasam, Geetha S., Karthik Dhatchinamoorthy, Mark Mattingly, Chris Seidel, and Jennifer L. Gerton. "Chromatin assembly factor-1 (CAF-1) chaperone regulates Cse4 deposition into chromatin in budding yeast." Nucleic Acids Research 46, no. 9 (March 7, 2018): 4440–55. http://dx.doi.org/10.1093/nar/gky169.

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Abstract Correct localization of the centromeric histone variant CenH3/CENP-A/Cse4 is an important part of faithful chromosome segregation. Mislocalization of CenH3 could affect chromosome segregation, DNA replication and transcription. CENP-A is often overexpressed and mislocalized in cancer genomes, but the underlying mechanisms are not understood. One major regulator of Cse4 deposition is Psh1, an E3 ubiquitin ligase that controls levels of Cse4 to prevent deposition into non-centromeric regions. We present evidence that Chromatin assembly factor-1 (CAF-1), an evolutionarily conserved histone H3/H4 chaperone with subunits shown previously to interact with CenH3 in flies and human cells, regulates Cse4 deposition in budding yeast. yCAF-1 interacts with Cse4 and can assemble Cse4 nucleosomes in vitro. Loss of yCAF-1 dramatically reduces the amount of Cse4 deposited into chromatin genome-wide when Cse4 is overexpressed. The incorporation of Cse4 genome-wide may have multifactorial effects on growth and gene expression. Loss of yCAF-1 can rescue growth defects and some changes in gene expression associated with Cse4 deposition that occur in the absence of Psh1-mediated proteolysis. Incorporation of Cse4 into promoter nucleosomes at transcriptionally active genes depends on yCAF-1. Overall our findings suggest CAF-1 can act as a CenH3 chaperone, regulating levels and incorporation of CenH3 in chromatin.

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50

Quiñones-Aguilar, Evangelina Esmeralda, Alfredo Reyes-Tena, Luis Guillermo Hernández-Montiel, and Gabriel Rincón Enríquez. "Bacteriófagos en el control biológico de Pseudomonas syringae pv. phaseolicola agente causal del tizón de halo del frijol." Ecosistemas y Recursos Agropecuarios 5, no. 14 (April 24, 2018): 191. http://dx.doi.org/10.19136/era.a5n14.1159.

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Pseudomonas syringae pv. phaseolicola (Psph) es el agente causal del tizón de halo del cultivo de frijol. El manejo de esta enfermedad está basado en antibióticos agrícolas o compuestos a base de cobre. Una alternativa es el control biológico con virus bacterianos (bacteriófagos). Por lo anterior, el objetivo del trabajo fue evaluar el efecto de bacteriófagos nativos del estado de Zacatecas en el control de cepas virulentas de Psph. Se realizaron tres experimentos: 1) se evaluó la patogenicidad y virulencia de seis cepas de Psph y la cepa de referencia 1448A en ejotes y plantas de frijol variedad Negro Bolita; 2) se evaluó la virulencia de las tres cepas más agresivas en la variedad Flor de Mayo que presenta mayor tolerancia al tizón de halo; y 3) se evaluaron siete bacteriófagos para determinar el control biológico del tizón en la cepa nativa Psph1 y la cepa 1448A en ejotes de frijol variedad Flor de Mayo. Se cuantificó el área del tizón de halo en mm2, se encontró que las seis cepas Psph nativas fueron patogénicas en ejotes y plantas de frijol; la virulencia de mayor a menor grado fue: 1448A (7.5 mm2); Psph67 (5.3 mm2) y Psph1 (3.8 mm2). Solo un bacteriófago (F2) redujo de forma signi cativa (p ≤ 0.05) un 60% el área provocada por la cepa 1448A en ejotes. Los resultados sugieren que la tecnología de los bacteriófagos podría ser una estrategia para el control biológico del tizón de halo del cultivo de frijol en la agricultura mexicana.

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