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DC Field | Value | Language |
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dc.citation.number | 4 | - |
dc.citation.startPage | e1000451 | - |
dc.citation.title | PLOS GENETICS | - |
dc.citation.volume | 5 | - |
dc.contributor.author | Moser, Sandra C. | - |
dc.contributor.author | von Elsner, Sophie | - |
dc.contributor.author | Buessing, Ingo | - |
dc.contributor.author | Alpi, Arno | - |
dc.contributor.author | Schnabel, Ralf | - |
dc.contributor.author | Gartner, Anton | - |
dc.date.accessioned | 2023-12-22T08:07:13Z | - |
dc.date.available | 2023-12-22T08:07:13Z | - |
dc.date.created | 2020-01-30 | - |
dc.date.issued | 2009-04 | - |
dc.description.abstract | CLK-2/TEL2 is essential for viability from yeasts to vertebrates, but its essential functions remain ill defined. CLK-2/TEL2 was initially implicated in telomere length regulation in budding yeast, but work in Caenorhabditis elegans has uncovered a function in DNA damage response signalling. Subsequently, DNA damage signalling defects associated with CLK-2/TEL2 have been confirmed in yeast and human cells. The CLK-2/TEL2 interaction with the ATM and ATR DNA damage sensor kinases and its requirement for their stability led to the proposal that CLK-2/TEL2 mutants might phenocopy ATM and/or ATR depletion. We use C. elegans to dissect developmental and cell cycle related roles of CLK-2. Temperature sensitive (ts) clk-2 mutants accumulate genomic instability and show a delay of embryonic cell cycle timing. This delay partially depends on the worm p53 homolog CEP-1 and is rescued by co-depletion of the DNA replication checkpoint proteins ATL-1 (C. elegans ATR) and CHK-1. In addition, clk-2 ts mutants show a spindle orientation defect in the eight cell stages that lead to major cell fate transitions. clk-2 deletion worms progress through embryogenesis and larval development by maternal rescue but become sterile and halt germ cell cycle progression. Unlike ATL-1 depleted germ cells, clk-2-null germ cells do not accumulate DNA double-strand breaks. Rather, clk-2 mutant germ cells arrest with duplicated centrosomes but without mitotic spindles in an early prophase like stage. This germ cell cycle arrest does not depend on cep-1, the DNA replication, or the spindle checkpoint. Our analysis shows that CLK-2 depletion does not phenocopy PIKK kinase depletion. Rather, we implicate CLK-2 in multiple developmental and cell cycle related processes and show that CLK-2 and ATR have antagonising functions during early C. elegans embryonic development. | - |
dc.identifier.bibliographicCitation | PLOS GENETICS, v.5, no.4, pp.e1000451 | - |
dc.identifier.doi | 10.1371/journal.pgen.1000451 | - |
dc.identifier.issn | 1553-7390 | - |
dc.identifier.scopusid | 2-s2.0-66149140649 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/31005 | - |
dc.identifier.url | https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000451 | - |
dc.identifier.wosid | 000266320200011 | - |
dc.language | 영어 | - |
dc.publisher | PUBLIC LIBRARY SCIENCE | - |
dc.title | Functional Dissection of Caenorhabditis elegans CLK-2/TEL2 Cell Cycle Defects during Embryogenesis and Germline Development | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Genetics & Heredity | - |
dc.relation.journalResearchArea | Genetics & Heredity | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordPlus | DAMAGE-INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | SPINDLE-ASSEMBLY CHECKPOINT | - |
dc.subject.keywordPlus | C-ELEGANS | - |
dc.subject.keywordPlus | DNA-DAMAGE | - |
dc.subject.keywordPlus | LIFE-SPAN | - |
dc.subject.keywordPlus | REPLICATION CHECKPOINT | - |
dc.subject.keywordPlus | PROTEIN-KINASE | - |
dc.subject.keywordPlus | EMBRYOS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | P53 | - |
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