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敲低甲藻凝聚素亚基会导致S期阻滞和液晶染色体解聚。

Knockdown of Dinoflagellate Condensin Subunit Leads to S-Phase Impediment and Decompaction of Liquid Crystalline Chromosomes.

作者信息

Yan Ting Hin Kosmo, Wu Zhihao, Kwok Alvin Chun Man, Wong Joseph Tin Yum

机构信息

Division of Life Science, Hong Kong University of Science & Technology, Clear Water Bay, Kowloon, Hong Kong Special Administrative Region, China.

出版信息

Microorganisms. 2020 Apr 14;8(4):565. doi: 10.3390/microorganisms8040565.

DOI:10.3390/microorganisms8040565
PMID:32295294
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7232253/
Abstract

Dinoflagellates have some of the largest genomes, and their liquid-crystalline chromosomes (LCCs) have high degrees of non-nucleosomal superhelicity with cation-mediated DNA condensation. It is currently unknown if condensins, pentameric protein complexes containing structural maintenance of chromosomes 2/4, commonly involved in eukaryotic chromosomes condensation in preparation for M phase, may be involved in the LCC structure. We find that CcSMC4p (dinoflagellate SMC4 homolog) level peaked at S/G2 phase, even though LCCs do not undergo global-decondensation for replication. Despite the differences in the chromosomal packaging system, heterologous CcSMC4p expression suppressed conditional lethality of the corresponding fission yeast mutant, suggesting conservation of some canonical condensin functions. CcSMC4p-knockdown led to sustained expression of the S-phase marker PCNAp, S-phase impediment, and distorted nuclei in the early stage of CcSMC4p depletion. Prolonged CcSMC4p-knockdown resulted in aneuploidal cells and nuclear swelling with increasing LCC decompaction-decondensation. Cumulatively, our data suggested CcSMC4p function was required for dinoflagellate S-phase progression, and we propose that condensin-mediated higher-order compaction provisioning is involved in the provision of local rigidity for the replisome.

摘要

甲藻拥有一些最大的基因组,其液晶染色体(LCCs)具有高度的非核小体超螺旋结构以及阳离子介导的DNA凝聚。目前尚不清楚凝聚素(一种包含染色体结构维持蛋白2/4的五聚体蛋白复合物,通常参与真核染色体在进入M期前的凝聚过程)是否参与LCC的结构形成。我们发现,尽管LCCs不会为了复制而进行整体解聚,但CcSMC4p(甲藻SMC4同源物)的水平在S/G2期达到峰值。尽管染色体包装系统存在差异,但异源CcSMC4p的表达抑制了相应裂殖酵母突变体的条件致死性,这表明一些典型的凝聚素功能具有保守性。敲低CcSMC4p会导致S期标记物PCNAp持续表达、S期受阻以及在CcSMC4p缺失早期细胞核变形。长期敲低CcSMC4p会导致非整倍体细胞以及细胞核肿胀,同时LCC的解压缩 - 解聚程度增加。总体而言,我们的数据表明CcSMC4p的功能对于甲藻S期进程是必需的,并且我们提出凝聚素介导的高阶压缩作用参与为复制体提供局部刚性。

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