Daughter-cell-specific modulation of nuclear pore complexes controls cell cycle entry during asymmetric division.
Daughter-cell-specific modulation of nuclear pore complexes controls cell cycle entry during asymmetric division.
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DOI：
10.1038/s41556-018-0056-9
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发表时间：
2018-04
影响因子：
21.3
通讯作者：
Mendoza M
中科院分区：
文献类型：
--
作者：
Kumar A;Sharma P;Gomar-Alba M;Shcheprova Z;Daulny A;Sanmartín T;Matucci I;Funaya C;Beato M;Mendoza M
细胞身份的获得与核周边和核孔复合体（NPC）的变化相关联。这些变化是否以及如何决定细胞命运仍不清楚。我们已经发现了一种调节NPC乙酰化的机制，以指导芽殖酵母不对称分裂后的细胞命运。赖氨酸脱乙酰酶Hos 3在有丝分裂期间特异性地与子细胞NPC结合以延迟细胞周期进入（开始）。核篮和中央通道核孔蛋白的Hos 3依赖性脱乙酰化建立了转录抑制因子Whi 5在后期的子细胞特异性核积累和CLN 2基因在随后的G1期的核周沉默。这两个事件的Hos 3依赖性协调抑制子细胞而不是母细胞中的启动。我们提出，去乙酰化调节转运依赖性和非依赖性功能的NPC，导致差异的母细胞和子细胞的细胞周期进程。类似的机制可能在多细胞生物体的特定细胞类型和/或细胞周期阶段调节NPC功能。
The acquisition of cellular identity is coupled to changes in the nuclear periphery and nuclear pore complexes (NPCs). Whether and how these changes determine cell fate remains unclear. We have uncovered a mechanism regulating NPC acetylation to direct cell fate after asymmetric division in budding yeast. The lysine deacetylase Hos3 associates specifically with daughter cell NPCs during mitosis to delay cell cycle entry (Start). Hos3-dependent deacetylation of nuclear basket and central channel nucleoporins establishes daughter cell-specific nuclear accumulation of the transcriptional repressor Whi5 during anaphase and perinuclear silencing of the CLN2 gene in the following G1 phase. Hos3-dependent coordination of both events restrains Start in daughter but not in mother cells. We propose that deacetylation modulates transport-dependent and -independent functions of NPCs, leading to differential cell cycle progression in mother and daughter cells. Similar mechanisms might regulate NPC functions in specific cell types and/or cell cycle stages in multicellular organisms.
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影响因子：
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作者：
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