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1

Hedlund, Petter. "Genes and erectile function." Current Opinion in Urology 13, no. 5 (September 2003): 397–403. http://dx.doi.org/10.1097/00042307-200309000-00007.

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2

Olfson, Emily, and David A. Ross. "Genes Orchestrating Brain Function." Biological Psychiatry 82, no. 3 (August 2017): e17-e19. http://dx.doi.org/10.1016/j.biopsych.2017.06.003.

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3

Sharon, Amir, Alin Finkelstein, Neta Shlezinger, and Ido Hatam. "Fungal apoptosis: function, genes and gene function." FEMS Microbiology Reviews 33, no. 5 (September 2009): 833–54. http://dx.doi.org/10.1111/j.1574-6976.2009.00180.x.

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4

Ishiura, S., S. Suo, and N. Sasagawa. "Genes involved in cognitive function." Seibutsu Butsuri 41, supplement (2001): S10. http://dx.doi.org/10.2142/biophys.41.s10_3.

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5

Ivanova, Elena, and Gavin Kelsey. "Imprinted genes and hypothalamic function." Journal of Molecular Endocrinology 47, no. 2 (July 28, 2011): R67—R74. http://dx.doi.org/10.1530/jme-11-0065.

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Genomic imprinting is an important and enigmatic form of gene regulation in mammals in which one copy of a gene is silenced in a manner determined by its parental history. Imprinted genes range from those with constitutive monoallelic silencing to those, typically more remote from imprinting control regions, that display developmentally regulated, tissue-specific or partial monoallelic expression. This diversity may make these genes, and the processes they control, more or less sensitive to factors that modify or disrupt epigenetic marks. Imprinted genes have important functions in development and physiology, including major endocrine/neuroendocrine axes. Owing to is central role in coordinating growth, metabolism and reproduction, as well as evidence from genetic and knockout studies, the hypothalamus may be a focus for imprinted gene action. Are there unifying principles that explain why a gene should be imprinted? Conflict between parental genomes over limiting maternal resources, but also co-adaptation between mothers and offspring, have been invoked to explain the evolution of imprinting. Recent reports suggest there may be many more genes imprinted in the hypothalamus than hitherto expected, and it will be important for these new candidates to be validated and to determine whether they conform to current notions of how imprinting is regulated. In fully evaluating the role of imprinted genes in the hypothalamus, much work needs to be done to identify the specific neuronal populations in which particular genes are expressed, establish whether there are pathways in common and whether imprinted genes are involved in long-term programming of hypothalamic functions.
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6

Davies, William, Phoebe M. Y. Lynn, Dinko Relkovic, and Lawrence S. Wilkinson. "Imprinted genes and neuroendocrine function." Frontiers in Neuroendocrinology 29, no. 3 (June 2008): 413–27. http://dx.doi.org/10.1016/j.yfrne.2007.12.001.

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7

Juszczak, Grzegorz R., and Adrian M. Stankiewicz. "Glucocorticoids, genes and brain function." Progress in Neuro-Psychopharmacology and Biological Psychiatry 82 (March 2018): 136–68. http://dx.doi.org/10.1016/j.pnpbp.2017.11.020.

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8

Thiem, Suzanne M. "Baculovirus genes affecting host function." In Vitro Cellular & Developmental Biology - Animal 45, no. 3-4 (February 27, 2009): 111–26. http://dx.doi.org/10.1007/s11626-008-9170-5.

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9

Fonseca, Ghislaine V., José Humberto M. Tambor, Marina P. Nobrega, Rafael Santos, and Francisco G. Nobrega. "Sugarcane genes related to mitochondrial function." Genetics and Molecular Biology 24, no. 1-4 (December 2001): 175–81. http://dx.doi.org/10.1590/s1415-47572001000100024.

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Mitochondria function as metabolic powerhouses by generating energy through oxidative phosphorylation and have become the focus of renewed interest due to progress in understanding the subtleties of their biogenesis and the discovery of the important roles which these organelles play in senescence, cell death and the assembly of iron-sulfur (Fe/S) centers. Using proteins from the yeast Saccharomyces cerevisiae, Homo sapiens and Arabidopsis thaliana we searched the sugarcane expressed sequence tag (SUCEST) database for the presence of expressed sequence tags (ESTs) with similarity to nuclear genes related to mitochondrial functions. Starting with 869 protein sequences, we searched for sugarcane EST counterparts to these proteins using the basic local alignment search tool TBLASTN similarity searching program run against 260,781 sugarcane ESTs contained in 81,223 clusters. We were able to recover 367 clusters likely to represent sugarcane orthologues of the corresponding genes from S. cerevisiae, H. sapiens and A. thaliana with E-value <= 10-10. Gene products belonging to all functional categories related to mitochondrial functions were found and this allowed us to produce an overview of the nuclear genes required for sugarcane mitochondrial biogenesis and function as well as providing a starting point for detailed analysis of sugarcane gene structure and physiology.
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10

Vieira, Elaine, Thomas P. Burris, and Ivan Quesada. "Clock genes, pancreatic function, and diabetes." Trends in Molecular Medicine 20, no. 12 (December 2014): 685–93. http://dx.doi.org/10.1016/j.molmed.2014.10.007.

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11

Frederickson, Robert. "Human genes find function in yeast." Nature Biotechnology 17, no. 9 (September 1999): 840. http://dx.doi.org/10.1038/12813.

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12

CHALEPAKIS, G., P. TREMBLAY, and P. GRUSS. "Pax genes, mutants and molecular function." Journal of Cell Science 1992, Supplement 16 (January 1, 1992): 61–67. http://dx.doi.org/10.1242/jcs.1992.supplement_16.8.

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13

Foronda, David, Luis F. de Navas, Daniel L. Garaulet, and Ernesto Sanchez-Herrero. "Function and specificity of Hox genes." International Journal of Developmental Biology 53, no. 8-9-10 (2009): 1404–19. http://dx.doi.org/10.1387/ijdb.072462df.

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14

Sýkorová, Eva, and Jiří Fajkus. "Structure-function relationships in telomerase genes." Biology of the Cell 101, no. 7 (July 2009): 375–406. http://dx.doi.org/10.1042/bc20080205.

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15

Boulin, Thomas, and Oliver Hobert. "From genes to function: theC.elegansgenetic toolbox." Wiley Interdisciplinary Reviews: Developmental Biology 1, no. 1 (November 28, 2011): 114–37. http://dx.doi.org/10.1002/wdev.1.

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16

Torres, Anthony R., Jonna B. Westover, and Allen J. Rosenspire. "HLA Immune Function Genes in Autism." Autism Research and Treatment 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/959073.

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The human leukocyte antigen (HLA) genes on chromosome 6 are instrumental in many innate and adaptive immune responses. The HLA genes/haplotypes can also be involved in immune dysfunction and autoimmune diseases. It is now becoming apparent that many of the non-antigen-presenting HLA genes make significant contributions to autoimmune diseases. Interestingly, it has been reported that autism subjects often have associations with HLA genes/haplotypes, suggesting an underlying dysregulation of the immune system mediated by HLA genes. Genetic studies have only succeeded in identifying autism-causing genes in a small number of subjects suggesting that the genome has not been adequately interrogated. Close examination of the HLA region in autism has been relatively ignored, largely due to extraordinary genetic complexity. It is our proposition that genetic polymorphisms in the HLA region, especially in the non-antigen-presenting regions, may be important in the etiology of autism in certain subjects.
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17

Ponce, Rita, Lene Martinsen, Luís M. Vicente, and Daniel L. Hartl. "Novel Genes from Formation to Function." International Journal of Evolutionary Biology 2012 (July 3, 2012): 1–9. http://dx.doi.org/10.1155/2012/821645.

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The study of the evolution of novel genes generally focuses on the formation of new coding sequences. However, equally important in the evolution of novel functional genes are the formation of regulatory regions that allow the expression of the genes and the effects of the new genes in the organism as well. Herein, we discuss the current knowledge on the evolution of novel functional genes, and we examine in more detail the youngest genes discovered. We examine the existing data on a very recent and rapidly evolving cluster of duplicated genes, the Sdic gene cluster. This cluster of genes is an excellent model for the evolution of novel genes, as it is very recent and may still be in the process of evolving.
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18

Merkeev, I. V., and A. A. Mironov. "Orphan genes: Function, evolution, and composition." Molecular Biology 42, no. 1 (February 2008): 127–32. http://dx.doi.org/10.1134/s0026893308010196.

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19

Willaredt, Marc A., Lena Ebbers, and Hans Gerd Nothwang. "Central auditory function of deafness genes." Hearing Research 312 (June 2014): 9–20. http://dx.doi.org/10.1016/j.heares.2014.02.004.

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20

Evans, Cory J., and Renato J. Aguilera. "DNase II: genes, enzymes and function." Gene 322 (December 2003): 1–15. http://dx.doi.org/10.1016/j.gene.2003.08.022.

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21

Lanahan, Anthony, and Paul Worley. "Immediate-Early Genes and Synaptic Function." Neurobiology of Learning and Memory 70, no. 1-2 (July 1998): 37–43. http://dx.doi.org/10.1006/nlme.1998.3836.

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22

Ross, Benjamin D., Leah Rosin, Andreas W. Thomae, Mary Alice Hiatt, Danielle Vermaak, Aida Flor A. de la Cruz, Axel Imhof, Barbara G. Mellone, and Harmit S. Malik. "Stepwise Evolution of Essential Centromere Function in a Drosophila Neogene." Science 340, no. 6137 (June 6, 2013): 1211–14. http://dx.doi.org/10.1126/science.1234393.

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Evolutionarily young genes that serve essential functions represent a paradox; they must perform a function that either was not required until after their birth or was redundant with another gene. How young genes rapidly acquire essential function is largely unknown. We traced the evolutionary steps by which the Drosophila gene Umbrea acquired an essential role in chromosome segregation in D. melanogaster since the gene's origin less than 15 million years ago. Umbrea neofunctionalization occurred via loss of an ancestral heterochromatin-localizing domain, followed by alterations that rewired its protein interaction network and led to species-specific centromere localization. Our evolutionary cell biology approach provides temporal and mechanistic detail about how young genes gain essential function. Such innovations may constantly alter the repertoire of centromeric proteins in eukaryotes.
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23

ITOH, MAKOTO, and LEON O. CHUA. "DESIGNING CNN GENES." International Journal of Bifurcation and Chaos 13, no. 10 (October 2003): 2739–824. http://dx.doi.org/10.1142/s0218127403008375.

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A systematic design methodology for finding CNN parameters with prescribed functions is proposed. A given function (task) is translated into several local operations, and they are realized as stable states of the CNN system. Many CNN parameters (CNN genes) with the same functions can be easily derived by using this design methodology. A genetic algorithm based CNN gene design methodology is also proposed. Two new genetic "activation and inactivation" operations are introduced to generate CNN genes effectively. Many useful CNN genes can be obtained systematically from known genes by using these genetic operations. Furthermore, the signal propagation property for activated and inactivated CNN genes is studied.
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24

Lawrence, Jeffrey G., and John R. Roth. "Selfish Operons: Horizontal Transfer May Drive the Evolution of Gene Clusters." Genetics 143, no. 4 (August 1, 1996): 1843–60. http://dx.doi.org/10.1093/genetics/143.4.1843.

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Abstract A model is presented whereby the formation of gene clusters in bacteria is mediated by transfer of DNA within and among taxa. Bacterial operons are typically composed of genes whose products contribute to a single function. If this function is subject to weak selection or to long periods with no selection, the contributing genes may accumulate mutations and be lost by genetic drift. From a cell's perspective, once several genes are lost, the function can be restored only if all missing genes were acquired simultaneously by lateral transfer. The probability of transfer of multiple genes increases when genes are physically proximate. From a gene's perspective, horizontal transfer provides a way to escape evolutionary loss by allowing colonization of organisms lacking the encoded functions. Since organisms bearing clustered genes are more likely to act as successful donors, clustered genes would spread among bacterial genomes. The physical proximity of genes may be considered a selfish property of the operon since it affects the probability of successful horizontal transfer but may provide no physiological benefit to the host. This process predicts a mosaic structure of modern genomes in which ancestral chromosomal material is interspersed with novel, horizontally transferred operons providing peripheral metabolic functions.
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25

Noble, Denis. "Genes and causation." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 366, no. 1878 (June 17, 2008): 3001–15. http://dx.doi.org/10.1098/rsta.2008.0086.

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Relating genotypes to phenotypes is problematic not only owing to the extreme complexity of the interactions between genes, proteins and high-level physiological functions but also because the paradigms for genetic causality in biological systems are seriously confused. This paper examines some of the misconceptions, starting with the changing definitions of a gene, from the cause of phenotype characters to the stretches of DNA. I then assess whether the ‘digital’ nature of DNA sequences guarantees primacy in causation compared to non-DNA inheritance, whether it is meaningful or useful to refer to genetic programs, and the role of high-level (downward) causation. The metaphors that served us well during the molecular biological phase of recent decades have limited or even misleading impacts in the multilevel world of systems biology. New paradigms are needed if we are to succeed in unravelling multifactorial genetic causation at higher levels of physiological function and so to explain the phenomena that genetics was originally about. Because it can solve the ‘genetic differential effect problem’, modelling of biological function has an essential role to play in unravelling genetic causation.
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26

Ramón-Cajal, Santiago, and Stefan Hümmer. "Beyond genes: Understanding the function of non coding DNA." ANALES RANM 135, no. 03 (January 2, 2019): 230–36. http://dx.doi.org/10.32440/ar.2018.135.03.rev04.

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27

KUSANO, Tomonobu, and Thomas BERBERICH. "Low-temperature-induced Genes and Their Function." JOURNAL OF THE BREWING SOCIETY OF JAPAN 89, no. 7 (1994): 505–12. http://dx.doi.org/10.6013/jbrewsocjapan1988.89.505.

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28

Bent, Andrew F. "Plant Disease Resistance Genes: Function Meets Structure." Plant Cell 8, no. 10 (October 1996): 1757. http://dx.doi.org/10.2307/3870228.

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29

Ogasawara, Naotake. "Systematic function analysis of Bacillus subtilis genes." Research in Microbiology 151, no. 2 (March 2000): 129–34. http://dx.doi.org/10.1016/s0923-2508(00)00118-2.

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30

Stuehr, Dennis J., and Jeannette Vasquez-Vivar. "Nitric oxide synthases-from genes to function." Nitric Oxide 63 (February 2017): 29. http://dx.doi.org/10.1016/j.niox.2017.01.005.

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31

Wylie, Annika, Amanda E. Jones, Alejandro D'Brot, Wan-Jin Lu, Paula Kurtz, John V. Moran, Dinesh Rakheja, et al. "p53 genes function to restrain mobile elements." Genes & Development 30, no. 1 (December 23, 2015): 64–77. http://dx.doi.org/10.1101/gad.266098.115.

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32

Sheldon, Stephen, and Philip Dyer. "HLA and MHC: Genes, molecules and function." Trends in Genetics 13, no. 2 (February 1997): 83–84. http://dx.doi.org/10.1016/s0168-9525(97)84647-1.

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33

Accolla, Roberto S. "HLA and MHC: Genes Molecules and function." Immunology Today 18, no. 4 (April 1997): 200–201. http://dx.doi.org/10.1016/s0167-5699(97)84671-3.

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34

Moss, Denis J., and Rajiv Khanna. "Major histocompatibility complex: from genes to function." Immunology Today 20, no. 4 (April 1999): 165–67. http://dx.doi.org/10.1016/s0167-5699(98)01389-9.

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35

Frankish, Helen. "Consortium uses RNAi to uncover genes' function." Lancet 361, no. 9357 (February 2003): 584. http://dx.doi.org/10.1016/s0140-6736(03)12552-4.

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36

Portas, Laura, Miguel Pereira, Seif O. Shaheen, Annah B. Wyss, Stephanie J. London, Peter G. J. Burney, Matthew Hind, Charlotte H. Dean, and Cosetta Minelli. "Lung Development Genes and Adult Lung Function." American Journal of Respiratory and Critical Care Medicine 202, no. 6 (September 15, 2020): 853–65. http://dx.doi.org/10.1164/rccm.201912-2338oc.

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37

Steinke, John W. "Can Genes Control Asthmatic Lung Function Patterns?" American Journal of Respiratory and Critical Care Medicine 194, no. 12 (December 15, 2016): 1439–40. http://dx.doi.org/10.1164/rccm.201607-1433ed.

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38

Mercier, Jean-Claude, and Jean-Luc Vilotte. "Structure and Function of Milk Protein Genes." Journal of Dairy Science 76, no. 10 (October 1993): 3079–98. http://dx.doi.org/10.3168/jds.s0022-0302(93)77647-x.

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39

Mikoshiba, K., H. Okano, T. A. Tamura, and K. Ikenaka. "Structure and Function of Myelin Protein Genes." Annual Review of Neuroscience 14, no. 1 (March 1991): 201–17. http://dx.doi.org/10.1146/annurev.ne.14.030191.001221.

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40

UOZUMI, Takeshi. "Structure and Function of Nitrogen Fixation Genes." Journal of the agricultural chemical society of Japan 67, no. 7 (1993): 1062–64. http://dx.doi.org/10.1271/nogeikagaku1924.67.1062.

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41

Raab, Jesse R., Jonathan Chiu, Jingchun Zhu, Sol Katzman, Sreenivasulu Kurukuti, Paul A. Wade, David Haussler, and Rohinton T. Kamakaka. "Human tRNA genes function as chromatin insulators." EMBO Journal 31, no. 2 (November 15, 2011): 330–50. http://dx.doi.org/10.1038/emboj.2011.406.

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42

Capecchi, Mario R. "Function of Homeobox Genes in SkeletAl Development." Annals of the New York Academy of Sciences 785, no. 1 (June 1996): 34–37. http://dx.doi.org/10.1111/j.1749-6632.1996.tb56241.x.

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43

FUKUHARA, Hiroshi. "Structure and function of yeast mitochondrial genes." Kagaku To Seibutsu 24, no. 11 (1986): 707–16. http://dx.doi.org/10.1271/kagakutoseibutsu1962.24.707.

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44

Göttfert, Michael. "Regulation and function of rhizobial nodulation genes." FEMS Microbiology Letters 104, no. 1-2 (January 1993): 39–63. http://dx.doi.org/10.1111/j.1574-6968.1993.tb05863.x.

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45

Li, Y. C. "Microsatellites Within Genes: Structure, Function, and Evolution." Molecular Biology and Evolution 21, no. 6 (February 12, 2004): 991–1007. http://dx.doi.org/10.1093/molbev/msh073.

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46

Carroll, Joanne M., Kwang Soo Kim, M. Elizabeth Ross, Marian J. Evinger, Soonjung L. Hahn, and Tong H. Joh. "Structure and function of catecholamine enzyme genes." Journal of the Autonomic Nervous System 33, no. 2 (May 1991): 129–30. http://dx.doi.org/10.1016/0165-1838(91)90160-5.

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47

de Bessa Garcia, Simone Aparecida, Mafalda Araújo, Tiago Pereira, João Mouta, and Renata Freitas. "HOX genes function in Breast Cancer development." Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1873, no. 2 (April 2020): 188358. http://dx.doi.org/10.1016/j.bbcan.2020.188358.

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48

McNatty, K. P., and K. M. Henderson. "Gonadotrophins, fecundity genes and ovarian follicular function." Journal of Steroid Biochemistry 27, no. 1-3 (January 1987): 365–73. http://dx.doi.org/10.1016/0022-4731(87)90329-3.

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49

Katsumura, Koichi Ricardo, Peng Liu, Charu Mehta, Kyle J. Hewitt, Alexandra Soukup, Isabela J. Fraga de Andrade, Erik A. Ranheim, Kirby D. Johnson, and Emery H. Bresnick. "Loss-of-Function and Gain-of-Function Consequences of GATA2 Disease Mutations." Blood 134, Supplement_1 (November 13, 2019): 2519. http://dx.doi.org/10.1182/blood-2019-129447.

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The master regulator of hematopoiesis GATA2 controls generation and function of hematopoietic stem and progenitor cells, and heterozygous GATA2 mutations create a predisposition to develop immunodeficiency, myelodysplasia, and acute myeloid leukemia (Spinner et al. Blood, 2014; Dickinson et al. Blood, 2014; Churpek and Bresnick J. Clin. Invest. 2019). Although mechanisms that trigger the transition of a non-pathogenic GATA2 mutation into overt pathology are enigmatic, a paradigm has arisen in which GATA2 mutations are considered to be loss-of-function. We developed a genetic rescue assay to quantify the function of wild type GATA2 and GATA2 disease mutants when expressed at near-physiological levels in primary progenitor cells and demonstrated that GATA2 disease mutations abrogate certain biological and molecular activities, while enabling others (Katsumura et al., 2018, PNAS). We isolated lineage-negative (Lin-) or Lin-Kit+ cells from fetal liver of mice with a homozygous mutation of the Gata2 -77 enhancer, which downregulates Gata2 expression by ~80%. The mutant progenitor cells are largely defective in erythroid, megakaryocytic and granulocytic differentiation and exhibit a predominant monocytic differentiation fate (Johnson et al., 2015, Science Adv.). We compared GATA2 and GATA2 disease mutant activities in the rescue system using a colony formation assay. GATA2, R307W mutant (in N-finger) and T354M mutant (in DNA-binding C-finger) rescued myeloid colony formation and promoted granulocyte proliferation. Surprisingly, R307W and T354M induced more CFU-GM than GATA2. GATA2 and R307W, but not T354M, rescued BFU-E. These data indicated that GATA2 disease mutations were not strictly inhibitory, and in certain contexts, mutant activities exceeded that of GATA2. To extend these results, we subjected -77+/+ or -77-/- Lin- cells to a short-term ex vivo liquid culture, expressed GATA2, R307W, or T354M and used RNA-seq to elucidate progenitor cell transcriptomes. While -77+/+ Lin- cells generate erythroid and myeloid cells, -77-/- Lin- cells are competent for myeloid, but not erythroid, differentiation. Comparison of -77+/+ and -77-/- cell transcriptomes revealed 3064 differentially expressed genes (>2-fold). 1824 genes were >2-fold higher in -77+/+ cells, and 1240 genes were >2-fold higher in -77-/- cells. GATA2 expression in -77-/- cells activated 834 genes >2-fold and repressed 503 genes >2-fold. 60-65% of these genes overlapped with genes differentially expressed between -77+/+ cells and -77-/- cells. R307W expression activated 661 genes >2-fold and repressed 523 genes >2-fold. T354M expression activated 468 genes >2-fold and repressed 575 genes >2-fold. The genes regulated by mutants included GATA2-regulated genes and certain genes that were not GATA2-regulated. Multiple genes were hypersensitive to the mutants, relative to GATA2, and the mutants ectopically regulated certain genes. However, R307W and T354M did not universally regulate an identical gene cohort. For example, both R307W and T354M activated Ncam1, Nrg4, and Mpo more strongly than GATA2. R307W, but not T354M, activated Ear2 and Ces1d more strongly than GATA2. By contrast, T354M, but not R307W, activated Ctsg, Epx, and Rab38 more strongly than GATA2. Both R307W and T354M repressed macrophage genes similarly to GATA2, but they lacked the capacity to activate mast cell genes, differing from GATA2. To elucidate molecular mechanisms underlying GATA2 mutant activities, we leveraged our prior discovery that p38 or ERK kinases induce multi-site GATA2 phosphorylation (Katsumura et al. Blood. 2017). We tested whether these kinases mediate the ectopic transcriptional regulatory activity of GATA2 disease mutants. p38 inhibition attenuated aberrant regulation of Ear2 and Ces1d by R307W (p < 0.05), and mutation of S192 to S192A decreased R307W-induced CFU-GM formation by 49% (p < 0.05). In aggregate, these results indicate that GATA2 disease mutants exert context-dependent activities to regulate transcription and differentiation, activities can be signal-dependent and certain activities are distinct from GATA2. It is attractive to consider the pathogenic consequences of GATA2 disease mutant gain-of-function activities, and an important implication is GATA2 mutation-associated hematologic diseases might not solely reflect haploinsufficiency. Disclosures No relevant conflicts of interest to declare.
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50

Sitnicka, Dorota, Katarzyna Figurska, and Slawomir Orzechowski. "Functional Analysis of Genes." Advances in Cell Biology 2, no. 1 (January 1, 2010): 1–16. http://dx.doi.org/10.2478/v10052-010-0001-y.

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SummaryThe aim of this article is to present the current literature concerning the expression analysis and methods of functional characteristics of genes. The progress in the analysis of gene expression within cells or whole tissues is undisputed and leads to a constant improvement of our understanding of the function of particular gene. The traditional methods of the functional characteristics of genes such as homology, inactivation and overexpression are more frequently being replaced by microarray and DNA chip analysis, which are extensively supported by bioinformatics tools. Knowledge of the functions and changes in gene expression has applications in medical diagnostics, the pharmaceutical industry and in plant and animal biotechnology.
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