Many genomic regions are required for normal embryonic programmed cell death in Caenorhabditis elegans.
Many genomic regions are required for normal embryonic programmed cell death in Caenorhabditis elegans.
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秀丽隐杆线虫正常胚胎程序性细胞死亡需要许多基因组区域。
DOI：
10.1093/genetics/158.1.237
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发表时间：
2001
期刊：
影响因子：
3.3
通讯作者：
Rothman,JH
中科院分区：
文献类型：
--
作者：
Sugimoto,A;Kusano,A;Hozak,RR;Derry,WB;Zhu,J;Rothman,JH
为了鉴定与秀丽隐杆线虫程序性细胞死亡（PCD）相关的基因，我们筛选了一组全面的染色体缺陷，以了解在胚胎发育过程中PCD模式的改变。从一组58个缺陷中，共去除约74%的基因组，鉴定出四个不同的类别。在I类（20个缺陷）中，在细胞尸体的时间模式上没有观察到与野生型的显著偏差，这表明大部分基因组不包含在胚胎PCD中发挥显着作用的合子基因。II类缺陷（16个缺陷定义了至少11个不同的基因组区域）导致没有或少于正常的细胞死亡。其中一些导致过早的细胞分裂阻滞，可能解释了细胞尸体数量的减少；然而，另一些对细胞增殖的影响很小，这表明细胞尸体数量的减少并不是过早胚胎停止的直接结果。在第三类（18个缺陷定义了至少16个独特的区域）中，观察到过量的细胞尸体。在III类缺陷中观察到的额外尸体的发育阶段各不相同，这表明在PCD中存在执行时间特异性功能的基因。IV类的四个缺陷（定义了至少三个独特的区域）显示出异常大的尸体，在某些情况下，这是由于细胞分裂过早停止而没有伴随的PCD阻滞。最后一类的缺陷表明，细胞死亡程序并不需要激活正常的胚胎细胞增殖，并且表明，虽然细胞分裂所需的一些基因也可能是细胞死亡所需的，但其他基因则不是。大多数由这些缺陷确定的区域不包含先前确定的合子细胞死亡基因。因此，正常的PCD线虫需要大量尚未鉴定的基因。
To identify genes involved in programmed cell death (PCD) inCaenorhabditis elegans, we screened a comprehensive set of chromosomal deficiencies for alterations in the pattern of PCD throughout embryonic development. From a set of 58 deficiencies, which collectively remove ∼74% of the genome, four distinct classes were identified. In class I (20 deficiencies), no significant deviation from wild type in the temporal pattern of cell corpses was observed, indicating that much of the genome does not contain zygotic genes that perform conspicuous roles in embryonic PCD. The class II deficiencies (16 deficiencies defining at least 11 distinct genomic regions) led to no or fewer-than-normal cell corpses. Some of these cause premature cell division arrest, probably explaining the diminution in cell corpse number; however, others have little effect on cell proliferation, indicating that the reduced cell corpse number is not a direct result of premature embryonic arrest. In class III (18 deficiencies defining at least 16 unique regions), an excess of cell corpses was observed. The developmental stage at which the extra corpses were observed varied among the class III deficiencies, suggesting the existence of genes that perform temporal-specific functions in PCD. The four deficiencies in class IV (defining at least three unique regions), showed unusually large corpses that were, in some cases, attributable to extremely premature arrest in cell division without a concomitant block in PCD. Deficiencies in this last class suggest that the cell death program does not require normal embryonic cell proliferation to be activated and suggest that while some genes required for cell division might also be required for cell death, others are not. Most of the regions identified by these deficiencies do not contain previously identified zygotic cell death genes. There are, therefore, a substantial number of as yet unidentified genes required for normal PCD inC. elegans.