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Tissue- and sex-specific small RNAomes reveal sex differences in response to the environment.组织和性别特异性的小 RNA 组揭示了环境响应中的性别差异。
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本文引用的文献

1
The SCF Slimb ubiquitin ligase regulates Plk4/Sak levels to block centriole reduplication.SCF Slimb泛素连接酶调节Plk4/Sak水平以阻止中心粒再复制。
J Cell Biol. 2009 Jan 26;184(2):225-39. doi: 10.1083/jcb.200808049.
2
The SCF/Slimb ubiquitin ligase limits centrosome amplification through degradation of SAK/PLK4.SCF/Slimb泛素连接酶通过降解SAK/PLK4来限制中心体扩增。
Curr Biol. 2009 Jan 13;19(1):43-9. doi: 10.1016/j.cub.2008.11.037. Epub 2008 Dec 11.
3
The conserved protein SZY-20 opposes the Plk4-related kinase ZYG-1 to limit centrosome size.保守蛋白SZY-20对抗与Plk4相关的激酶ZYG-1以限制中心体大小。
Dev Cell. 2008 Dec;15(6):901-12. doi: 10.1016/j.devcel.2008.09.018.
4
Centrosome amplification can initiate tumorigenesis in flies.中心体扩增可在果蝇中引发肿瘤发生。
Cell. 2008 Jun 13;133(6):1032-42. doi: 10.1016/j.cell.2008.05.039.
5
Drosophila SPD-2 is an essential centriole component required for PCM recruitment and astral-microtubule nucleation.果蝇SPD-2是一种中心粒必需成分,是募集中心体周边物质(PCM)和星状微管成核所必需的。
Curr Biol. 2008 Feb 26;18(4):303-9. doi: 10.1016/j.cub.2008.01.058.
6
The mammalian SPD-2 ortholog Cep192 regulates centrosome biogenesis.哺乳动物SPD-2的直系同源物Cep192调控中心体生物发生。
Curr Biol. 2008 Jan 22;18(2):136-41. doi: 10.1016/j.cub.2007.12.055.
7
SAS-6 is a cartwheel protein that establishes the 9-fold symmetry of the centriole.SAS-6是一种形成中心粒九重对称性的轮状蛋白。
Curr Biol. 2007 Dec 18;17(24):2169-74. doi: 10.1016/j.cub.2007.11.046.
8
Spermatogenesis.精子发生
WormBook. 2006 Feb 20:1-14. doi: 10.1895/wormbook.1.85.1.
9
Human Cep192 is required for mitotic centrosome and spindle assembly.人类的Cep192是有丝分裂中心体和纺锤体组装所必需的。
Curr Biol. 2007 Nov 20;17(22):1960-6. doi: 10.1016/j.cub.2007.10.019. Epub 2007 Nov 1.
10
The zebrafish maternal-effect gene cellular atoll encodes the centriolar component sas-6 and defects in its paternal function promote whole genome duplication.斑马鱼母体效应基因“细胞环礁”编码中心粒成分sas-6,其父本功能缺陷会促进全基因组复制。
Dev Biol. 2007 Dec 1;312(1):44-60. doi: 10.1016/j.ydbio.2007.08.054. Epub 2007 Sep 7.

Plk4 相关激酶 ZYG-1 对有丝分裂和减数分裂中心体复制的控制。

Control of mitotic and meiotic centriole duplication by the Plk4-related kinase ZYG-1.

机构信息

Laboratory of Biochemistry and Genetics, NIDDK/NIH, Bethesda, MD 20892, USA.

出版信息

J Cell Sci. 2010 Mar 1;123(Pt 5):795-805. doi: 10.1242/jcs.050682. Epub 2010 Feb 9.

DOI:10.1242/jcs.050682
PMID:20144993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2823580/
Abstract

Centriole duplication is of crucial importance during both mitotic and male meiotic divisions, but it is currently not known whether this process is regulated differently during the two modes of division. In Caenorhabditis elegans, the kinase ZYG-1 plays an essential role in both mitotic and meiotic centriole duplication. We have found that the C-terminus of ZYG-1 is necessary and sufficient for targeting to centrosomes and is important for differentiating mitotic and meiotic centriole duplication. Small truncations of the C-terminus dramatically lower the level of ZYG-1 at mitotic centrosomes but have little effect on the level of ZYG-1 at meiotic centrosomes. Interestingly, truncation of ZYG-1 blocks centrosome duplication in the mitotic cycle but leads to centrosome amplification in the meiotic cycle. Meiotic centriole amplification appears to result from the overduplication of centrioles during meiosis I and leads to the formation of multipolar meiosis II spindles. The extra centrioles also disrupt spermatogenesis by inducing the formation of supernumerary fertilization-competent spermatids that contain abnormal numbers of chromosomes and centrioles. Our data reveal differences in the regulation of mitotic and meiotic centrosome duplication, particularly with regard to ZYG-1 activity, and reveal an important role for centrosomes in spermatid formation.

摘要

中心体复制对于有丝分裂和雄性减数分裂都至关重要,但目前尚不清楚这个过程在这两种分裂方式中是否受到不同的调节。在秀丽隐杆线虫中,激酶 ZYG-1 在有丝分裂和减数分裂中心体复制中都发挥着重要作用。我们发现 ZYG-1 的 C 端对于定位于中心体是必要且充分的,并且对于区分有丝分裂和减数分裂中心体复制很重要。C 端的小截断大大降低了有丝分裂中心体中 ZYG-1 的水平,但对减数分裂中心体中 ZYG-1 的水平几乎没有影响。有趣的是,ZYG-1 的截断会阻断有丝分裂周期中的中心体复制,但会导致减数分裂周期中的中心体扩增。减数分裂中心体扩增似乎是由于减数分裂 I 期间中心体的过度复制导致的,导致多极减数分裂 II 纺锤体的形成。额外的中心体还通过诱导形成具有异常数量的染色体和中心体的多余有受精能力的精子来干扰精子发生。我们的数据揭示了有丝分裂和减数分裂中心体复制的调节差异,特别是 ZYG-1 活性的差异,并揭示了中心体在精子形成中的重要作用。