[{"date_created":"2024-10-09T07:44:48Z","status":"public","issue":"5","citation":{"short":"A.M. Bronstein, S. Bramson, K. Shemesh, B. Liefshitz, M. Kupiec, G3: Genes, Genomes, Genetics  8 (2018) 1615–1626.","chicago":"Bronstein, Alex M., Shay Bramson, Keren Shemesh, Batia Liefshitz, and Martin Kupiec. “Tight Regulation of Srs2 Helicase Activity Is Crucial for Proper Functioning of DNA Repair Mechanisms.” <i>G3: Genes, Genomes, Genetics </i>. Oxford University Press (OUP), 2018. <a href=\"https://doi.org/10.1534/g3.118.200181\">https://doi.org/10.1534/g3.118.200181</a>.","ista":"Bronstein AM, Bramson S, Shemesh K, Liefshitz B, Kupiec M. 2018. Tight regulation of Srs2 helicase activity is crucial for proper functioning of DNA Repair mechanisms. G3: Genes, Genomes, Genetics . 8(5), 1615–1626.","ama":"Bronstein AM, Bramson S, Shemesh K, Liefshitz B, Kupiec M. Tight regulation of Srs2 helicase activity is crucial for proper functioning of DNA Repair mechanisms. <i>G3: Genes, Genomes, Genetics </i>. 2018;8(5):1615-1626. doi:<a href=\"https://doi.org/10.1534/g3.118.200181\">10.1534/g3.118.200181</a>","mla":"Bronstein, Alex M., et al. “Tight Regulation of Srs2 Helicase Activity Is Crucial for Proper Functioning of DNA Repair Mechanisms.” <i>G3: Genes, Genomes, Genetics </i>, vol. 8, no. 5, Oxford University Press (OUP), 2018, pp. 1615–26, doi:<a href=\"https://doi.org/10.1534/g3.118.200181\">10.1534/g3.118.200181</a>.","ieee":"A. M. Bronstein, S. Bramson, K. Shemesh, B. Liefshitz, and M. Kupiec, “Tight regulation of Srs2 helicase activity is crucial for proper functioning of DNA Repair mechanisms,” <i>G3: Genes, Genomes, Genetics </i>, vol. 8, no. 5. Oxford University Press (OUP), pp. 1615–1626, 2018.","apa":"Bronstein, A. M., Bramson, S., Shemesh, K., Liefshitz, B., &#38; Kupiec, M. (2018). Tight regulation of Srs2 helicase activity is crucial for proper functioning of DNA Repair mechanisms. <i>G3: Genes, Genomes, Genetics </i>. Oxford University Press (OUP). <a href=\"https://doi.org/10.1534/g3.118.200181\">https://doi.org/10.1534/g3.118.200181</a>"},"month":"05","language":[{"iso":"eng"}],"volume":8,"doi":"10.1534/g3.118.200181","article_processing_charge":"No","_id":"18277","quality_controlled":"1","oa":1,"extern":"1","scopus_import":"1","year":"2018","publisher":"Oxford University Press (OUP)","title":"Tight regulation of Srs2 helicase activity is crucial for proper functioning of DNA Repair mechanisms","abstract":[{"lang":"eng","text":"Proper DNA damage repair is one of the most vital and fundamental functions of every cell. Several different repair mechanisms exist to deal with various types of DNA damage, in various stages of the cell cycle and under different conditions. Homologous recombination is one of the most important repair mechanisms in all organisms. Srs2, a regulator of homologous recombination, is a DNA helicase involved in DNA repair, cell cycle progression and genome integrity. Srs2 can remove Rad51 from ssDNA, and is thought to inhibit unscheduled recombination. However, Srs2 has to be precisely regulated, as failure to do so is toxic and can lead to cell death. We noticed that a very slight elevation of the levels of Srs2 (by addition of a single extra copy of the SRS2 gene) leads to hyper-sensitivity of yeast cells to methyl methanesulfonate (MMS, a DNA damaging agent). This effect is seen in haploid, but not in diploid, cells. We analyzed the mechanism that controls haploid/diploid sensitivity and arrived to the conclusion that the sensitivity requires the activity of RAD59 and RDH54, whose expression in diploid cells is repressed. We carried out a mutational analysis of Srs2 to determine the regions of the protein required for the sensitization to genotoxins. Interestingly, Srs2 needs the HR machinery and its helicase activity for its toxicity, but does not need to dismantle Rad51. Our work underscores the tight regulation that is required on the levels of Srs2 activity, and the fact that Srs2 helicase activity plays a more central role in DNA repair than the ability of Srs2 to dismantle Rad51 filaments."}],"publication_status":"published","intvolume":"         8","DOAJ_listed":"1","date_published":"2018-05-01T00:00:00Z","day":"01","page":"1615-1626","type":"journal_article","publication":"G3: Genes, Genomes, Genetics ","date_updated":"2024-12-19T16:00:24Z","author":[{"orcid":"0000-0001-9699-8730","last_name":"Bronstein","id":"58f3726e-7cba-11ef-ad8b-e6e8cb3904e6","full_name":"Bronstein, Alexander","first_name":"Alexander"},{"full_name":"Bramson, Shay","first_name":"Shay","last_name":"Bramson"},{"first_name":"Keren","full_name":"Shemesh, Keren","last_name":"Shemesh"},{"last_name":"Liefshitz","full_name":"Liefshitz, Batia","first_name":"Batia"},{"full_name":"Kupiec, Martin","first_name":"Martin","last_name":"Kupiec"}],"publication_identifier":{"eissn":["2160-1836"]},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1534/g3.118.200181"}],"oa_version":"Published Version"},{"abstract":[{"lang":"eng","text":"\r\n\r\nElg1 and Srs2 are two proteins involved in maintaining genome stability in yeast. After DNA damage, the homotrimeric clamp PCNA, which provides stability and processivity to DNA polymerases and serves as a docking platform for DNA repair enzymes, undergoes modification by the ubiquitin-like molecule SUMO. PCNA SUMOylation helps recruit Srs2 and Elg1 to the replication fork. In the absence of Elg1, both SUMOylated PCNA and Srs2 accumulate at the chromatin fraction, indicating that Elg1 is required for removing SUMOylated PCNA and Srs2 from DNA. Despite this interaction, which suggests that the two proteins work together, double mutants elg1Δ srs2Δ have severely impaired growth as haploids and exhibit synergistic sensitivity to DNA damage and a synergistic increase in gene conversion. In addition, diploid elg1Δ srs2Δ double mutants are dead, which implies that an essential function in the cell requires at least one of the two gene products for survival. To gain information about this essential function, we have carried out a high copy number suppressor screen to search for genes that, when overexpressed, suppress the synthetic lethality between elg1Δ and srs2Δ. We report the identification of 36 such genes, which are enriched for functions related to DNA- and chromatin-binding, chromatin packaging and modification, and mRNA export from the nucleus."}],"title":"A genetic screen for high copy number suppressors of the synthetic lethality between elg1Δ and srs2Δ in yeast","publisher":"Oxford University Press","scopus_import":"1","year":"2013","extern":"1","oa":1,"_id":"18437","quality_controlled":"1","article_processing_charge":"No","doi":"10.1534/g3.113.005561","language":[{"iso":"eng"}],"volume":3,"issue":"5","citation":{"chicago":"Gazy, Inbal, Batia Liefshitz, Alex M. Bronstein, Oren Parnas, Nir Atias, Roded Sharan, and Martin Kupiec. “A Genetic Screen for High Copy Number Suppressors of the Synthetic Lethality between Elg1Δ and Srs2Δ in Yeast.” <i> G3: Genes, Genomes, Genetics</i>. Oxford University Press, 2013. <a href=\"https://doi.org/10.1534/g3.113.005561\">https://doi.org/10.1534/g3.113.005561</a>.","ista":"Gazy I, Liefshitz B, Bronstein AM, Parnas O, Atias N, Sharan R, Kupiec M. 2013. A genetic screen for high copy number suppressors of the synthetic lethality between elg1Δ and srs2Δ in yeast.  G3: Genes, Genomes, Genetics. 3(5), 917–926.","short":"I. Gazy, B. Liefshitz, A.M. Bronstein, O. Parnas, N. Atias, R. Sharan, M. Kupiec,  G3: Genes, Genomes, Genetics 3 (2013) 917–926.","apa":"Gazy, I., Liefshitz, B., Bronstein, A. M., Parnas, O., Atias, N., Sharan, R., &#38; Kupiec, M. (2013). A genetic screen for high copy number suppressors of the synthetic lethality between elg1Δ and srs2Δ in yeast. <i> G3: Genes, Genomes, Genetics</i>. Oxford University Press. <a href=\"https://doi.org/10.1534/g3.113.005561\">https://doi.org/10.1534/g3.113.005561</a>","ieee":"I. Gazy <i>et al.</i>, “A genetic screen for high copy number suppressors of the synthetic lethality between elg1Δ and srs2Δ in yeast,” <i> G3: Genes, Genomes, Genetics</i>, vol. 3, no. 5. Oxford University Press, pp. 917–926, 2013.","mla":"Gazy, Inbal, et al. “A Genetic Screen for High Copy Number Suppressors of the Synthetic Lethality between Elg1Δ and Srs2Δ in Yeast.” <i> G3: Genes, Genomes, Genetics</i>, vol. 3, no. 5, Oxford University Press, 2013, pp. 917–26, doi:<a href=\"https://doi.org/10.1534/g3.113.005561\">10.1534/g3.113.005561</a>.","ama":"Gazy I, Liefshitz B, Bronstein AM, et al. A genetic screen for high copy number suppressors of the synthetic lethality between elg1Δ and srs2Δ in yeast. <i> G3: Genes, Genomes, Genetics</i>. 2013;3(5):917-926. doi:<a href=\"https://doi.org/10.1534/g3.113.005561\">10.1534/g3.113.005561</a>"},"month":"05","date_created":"2024-10-15T11:20:55Z","status":"public","main_file_link":[{"url":"https://doi.org/10.1534/g3.113.005561","open_access":"1"}],"oa_version":"Published Version","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","author":[{"last_name":"Gazy","full_name":"Gazy, Inbal","first_name":"Inbal"},{"last_name":"Liefshitz","full_name":"Liefshitz, Batia","first_name":"Batia"},{"first_name":"Alexander","full_name":"Bronstein, Alexander","orcid":"0000-0001-9699-8730","last_name":"Bronstein","id":"58f3726e-7cba-11ef-ad8b-e6e8cb3904e6"},{"first_name":"Oren","full_name":"Parnas, Oren","last_name":"Parnas"},{"last_name":"Atias","full_name":"Atias, Nir","first_name":"Nir"},{"full_name":"Sharan, Roded","first_name":"Roded","last_name":"Sharan"},{"first_name":"Martin","full_name":"Kupiec, Martin","last_name":"Kupiec"}],"publication_identifier":{"eissn":["2160-1836"]},"date_updated":"2024-12-18T15:30:20Z","publication":" G3: Genes, Genomes, Genetics","type":"journal_article","page":"917-926","day":"01","date_published":"2013-05-01T00:00:00Z","DOAJ_listed":"1","intvolume":"         3","publication_status":"published"}]