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首页> 外文期刊>Current Biology: CB >Absence of the Spindle Assembly Checkpoint Restores Mitotic Fidelity upon Loss of Sister Chromatid Cohesion
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Absence of the Spindle Assembly Checkpoint Restores Mitotic Fidelity upon Loss of Sister Chromatid Cohesion

机译：缺乏主轴组件检查点恢复有丝分裂保真度，减少姐妹染色体凝聚力

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The fidelity of mitosis depends on cohesive forces that keep sister chromatids together. This is mediated by cohesin that embraces sister chromatid fibers from the time of their replication until the subsequent mitosis []. Cleavage of cohesin marks anaphase onset, where single chromatids are dragged to the poles by the mitotic spindle []. Cohesin cleavage should only occur when all chromosomes are properly bio-oriented to ensure equal genome distribution and prevent random chromosome segregation. Unscheduled loss of sister chromatid cohesion is prevented by a safeguard mechanism known as the spindle assembly checkpoint (SAC) []. To identify specific conditions capable of restoring defects associated with cohesion loss, we screened for genes whose depletion modulatesDrosophilawing development when sister chromatid cohesion is impaired. Cohesion deficiency was induced by knockdown of?the acetyltransferase separation anxiety (San)/Naa50, a cohesin complex stabilizer []. Several genes whose function impacts wing development upon cohesion loss were identified. Surprisingly, knockdown of key SAC proteins, Mad2 and Mps1, suppressed developmental defects associated with San depletion. SAC impairment upon cohesin removal, triggered by San depletion or artificial removal of the cohesin complex, prevented extensive genome shuffling, reduced segregation defects, and restored cell survival. This counterintuitive phenotypic suppression was caused by an intrinsic bias for efficient chromosome biorientation at mitotic entry, coupled with slow engagement of error-correction reactions. Thus, in contrast to SAC’s role as a safeguard mechanism for mitotic fidelity, removal of this checkpoint alleviates mitotic errors when sister chromatid cohesion is compromised.
机译：有丝分裂的保真取决于将姐妹染色体一起保持的粘性力量。这是由Cohesin介导的，这些凝聚在其复制中的姐妹染色体纤维直至随后的丝分裂[]。 Cohyin的裂解标记术语术，其中单个染色体被丝状纺锤体拖到杆子上。只有当所有染色体正确的生物学导向时都应该仅发生休谷蛋白裂解，以确保相等的基因组分布并防止随机染色体隔离。通过称为主轴组件检查点（SAC）[]的保障机制，防止了未核化的乳腺染色体内聚力的丧失。为了鉴定能够恢复与粘性损失相关的缺陷的特定条件，我们筛选出缺乏调节液体干燥的基因，当患者染色体粘性内粘性受到损害时。通过敲低诱导凝聚力缺陷？乙酰转移酶分离焦虑（SAN）/ NaA50，Cohyin复合稳定剂[]。鉴定了功能影响机翼开发的几个基因。令人惊讶的是，关键囊蛋白，MAD2和MPS1的敲低，抑制了与SAN耗尽相关的发育缺陷。囊型损伤在休谷蛋白上，由San耗尽或人工去除休息络合物，防止了广泛的基因组洗涤，降低的偏析缺陷，并恢复细胞存活。该逆向表型抑制是由有丝分裂入口处的有效染色体展开的内在偏差引起的，再加上误差校正反应的缓慢接合。因此，与SAC作为有丝分裂保真度的保障机制相比，当患者染色体内聚力受到损害时，去除该检查点减轻了有丝分裂误差。

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