Treslin, DUE-B, and GEMC1 cannot complement Sld3 mutants in fission yeast.
Treslin, DUE-B, and GEMC1 cannot complement Sld3 mutants in fission yeast.
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Treslin、DUE-B 和 GEMC1 不能补充裂殖酵母中的 Sld3 突变体。
DOI:
10.1111/j.1567-1364.2012.00794.x
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发表时间:
2012
影响因子:
3.2
通讯作者:
Xu,Yong-Jie
中科院分区:
文献类型:
--
作者:
Wang,Zhuo;Kim,Elaine;Leffak,Michael;Xu,Yong-Jie
Initiation of DNA replication in eukaryotes is an evolutionarily conserved process that involves two distinct steps: the formation of prereplication complexes at replication origins in G1 and the assembly of preinitiation complexes (pre-ICs) in S phase, which leads to activation of the replication helicase. For the assembly of pre-ICs in yeast, formation of the Sld2–Dpb11–Sld3 complex is a critical event that requires phosphorylation of Sld2 and Sld3 by cyclin-dependent kinase. In mammals, RecQL4 and TopBP1 are excellent ortholog candidates for Sld2 and Dpb11, respectively. In this past year, three TopBP1-interacting proteins Treslin/Ticrr, GEMC1, and DUE-B have been identified in metazoans as possible functional orthologs of the yeast Sld3. To test this hypothesis, we carried out several complementation tests in fission yeast. The proteins were expressed at various levels in the temperature-sensitivesld3-10mutant and in cells that lack endogenous Sld3. Our result showed that none of these metazoan proteins could rescue growth defect of thesld3mutants. Although the result may have several interpretations, it is possible that the helicase activation in mammals has diverged in complexity during evolution from that in yeasts and may involve multiple players that interact with TopBP1.
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影响因子:
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通讯作者:
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