Differential processing of leading- and lagging-strand ends at Saccharomyces cerevisiae telomeres revealed by the absence of Rad27p nuclease. Export

@article{citeulike:1177612, abstract = {Saccharomyces cerevisiae strains lacking the Rad27p nuclease, a homolog of the mammalian FEN-1 protein, display an accumulation of extensive single-stranded G-tails at telomeres. Furthermore, the lengths of telomeric repeats become very heterogeneous. These phenotypes could be the result of aberrant Okazaki fragment processing of the C-rich strand, elongation of the G-rich strand by telomerase, or an abnormally high activity of the nucleolytic activities required to process leading-strand ends. To distinguish among these possibilities, we analyzed strains carrying a deletion of the RAD27 gene and also lacking genes required for in vivo telomerase activity. The results show that double-mutant strains died more rapidly than strains lacking only telomerase components. Furthermore, in such strains there is a significant reduction in the signals for G-tails as compared to those detected in rad27delta cells. The results from studies of the replication intermediates of a linear plasmid in rad27delta cells are consistent with the idea that only one end of the plasmid acquires extensive G-tails, presumably the end made by lagging-strand synthesis. These data further support the notion that chromosome ends have differential requirements for end processing, depending on whether the ends were replicated by leading- or lagging-strand synthesis.}, address = {D\'{e}partement de Microbiologie et Infectiologie, Facult\'{e} de M\'{e}decine, Universit\'{e} de Sherbooke, Sherbooke, Quebec J1H 5N4, Canada.}, author = {Parenteau, J. and Wellinger, R. J.}, citeulike-article-id = {1177612}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/12524334}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=12524334}, issn = {0016-6731}, journal = {Genetics}, keywords = {capping, rad27p, replication}, month = {December}, number = {4}, pages = {1583--1594}, posted-at = {2007-03-20 15:15:47}, priority = {4}, title = {Differential processing of leading- and lagging-strand ends at Saccharomyces cerevisiae telomeres revealed by the absence of Rad27p nuclease.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/12524334}, volume = {162}, year = {2002} }

TY - JOUR ID - citeulike:1177612 L3 - citeulike-article-id:1177612 N2 - Saccharomyces cerevisiae strains lacking the Rad27p nuclease, a homolog of the mammalian FEN-1 protein, display an accumulation of extensive single-stranded G-tails at telomeres. Furthermore, the lengths of telomeric repeats become very heterogeneous. These phenotypes could be the result of aberrant Okazaki fragment processing of the C-rich strand, elongation of the G-rich strand by telomerase, or an abnormally high activity of the nucleolytic activities required to process leading-strand ends. To distinguish among these possibilities, we analyzed strains carrying a deletion of the RAD27 gene and also lacking genes required for in vivo telomerase activity. The results show that double-mutant strains died more rapidly than strains lacking only telomerase components. Furthermore, in such strains there is a significant reduction in the signals for G-tails as compared to those detected in rad27delta cells. The results from studies of the replication intermediates of a linear plasmid in rad27delta cells are consistent with the idea that only one end of the plasmid acquires extensive G-tails, presumably the end made by lagging-strand synthesis. These data further support the notion that chromosome ends have differential requirements for end processing, depending on whether the ends were replicated by leading- or lagging-strand synthesis. IS - 4 JF - Genetics SN - 0016-6731 AD - Département de Microbiologie et Infectiologie, Faculté de Médecine, Université de Sherbooke, Sherbooke, Quebec J1H 5N4, Canada. EP - 1594 TI - Differential processing of leading- and lagging-strand ends at Saccharomyces cerevisiae telomeres revealed by the absence of Rad27p nuclease. VL - 162 SP - 1583 KW - capping KW - rad27p KW - replication AU - Parenteau, J AU - Wellinger, RJ PY - 2002/12// UR - http://view.ncbi.nlm.nih.gov/pubmed/12524334 ER -