NPP-16/Nup50 function and CDK-1 inactivation are associated with anoxia-induced prophase arrest in Caenorhabditis elegans.
NPP-16/Nup50 function and CDK-1 inactivation are associated with anoxia-induced prophase arrest in Caenorhabditis elegans.
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DOI:
10.1091/mbc.e09-09-0787
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发表时间:
2010-03-01
影响因子:
3.3
通讯作者:
Padilla PA
中科院分区:
文献类型:
--
作者:
Hajeri VA;Little BA;Ladage ML;Padilla PA
Cellular and genetic analysis supports the notion that NPP-16/NUP50 and CDK-1 function to reversibly arrest prophase blastomeres in Caenorhabditis elegans embryos exposed to anoxia. The anoxia-induced shift of cells from an actively dividing state to an arrested state reveals a previously uncharacterized prophase checkpoint in the C. elegans embryo. Oxygen, an essential nutrient, is sensed by a multiple of cellular pathways that facilitate the responses to and survival of oxygen deprivation. The Caenorhabditis elegans embryo exposed to severe oxygen deprivation (anoxia) enters a state of suspended animation in which cell cycle progression reversibly arrests at specific stages. The mechanisms regulating interphase, prophase, or metaphase arrest in response to anoxia are not completely understood. Characteristics of arrested prophase blastomeres and oocytes are the alignment of condensed chromosomes at the nuclear periphery and an arrest of nuclear envelope breakdown. Notably, anoxia-induced prophase arrest is suppressed in mutant embryos lacking nucleoporin NPP-16/NUP50 function, indicating that this nucleoporin plays an important role in prophase arrest in wild-type embryos. Although the inactive form of cyclin-dependent kinase (CDK-1) is detected in wild-type–arrested prophase blastomeres, the inactive state is not detected in the anoxia exposed npp-16 mutant. Furthermore, we found that CDK-1 localizes near chromosomes in anoxia-exposed embryos. These data support the notion that NPP-16 and CDK-1 function to arrest prophase blastomeres in C. elegans embryos. The anoxia-induced shift of cells from an actively dividing state to an arrested state reveals a previously uncharacterized prophase checkpoint in the C. elegans embryo.
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影响因子:
64.8
作者:
Cahill, DP;Lengauer, C;Vogelstein, B
通讯作者:
Vogelstein, B
影响因子:
3.3
作者:
Encalada, SE;Willis, J;Bowerman, B
通讯作者:
Bowerman, B
DOI:
10.1083/jcb.100.5.1623
发表时间:
1985-05
期刊:
The Journal of cell biology
影响因子:
--
作者:
Foe VE;Alberts BM
通讯作者:
Alberts BM
DOI:
10.1152/ajpregu.2001.280.5.r1555
发表时间:
2001-05-01
影响因子:
2.8
作者:
Douglas, RM;Xu, T;Haddad, GG
通讯作者:
Haddad, GG
影响因子:
64.8
作者:
Buchwitz, BJ;Ahmad, K;Henikoff, S
通讯作者:
Henikoff, S