Euling S, Ambros V
Department of Cellular and Developmental Biology, Harvard University Cambridge, Massachusetts 02138, USA.
Cell. 1996 Mar 8;84(5):667-76. doi: 10.1016/s0092-8674(00)81045-4.
Heterochronic genes control the timing of vulval development in the C. elegans hermaphrodite. lin-14 or lin-28 loss-of-function mutations cause the vulval precursor cells (VPCs) to enter S phase and to divide one larval stage earlier than in the wild type. A precocious vulva is formed by essentially normal cell lineage patterns, governed by the same intercellular signals as in the wild type. Mutations that prevent the normal developmental down-regulation of lin-14, activity delay or block VPC division and prevent vulval differentiation. A genetic pathway that includes lin-4, lin-14, and lin-28 controls when VPCs complete G1 and also controls when VPCs acquire the competence to respond to the intercellular patterning signals and express vulval fates.
异时基因控制秀丽隐杆线虫雌雄同体中阴门发育的时间。lin-14或lin-28功能丧失突变会导致阴门前体细胞(VPCs)进入S期,并比野生型早一个幼虫阶段进行分裂。早熟的阴门由基本正常的细胞谱系模式形成,受与野生型相同的细胞间信号调控。阻止lin-14活性正常发育性下调的突变会延迟或阻断VPC分裂,并阻止阴门分化。包括lin-4、lin-14和lin-28的遗传途径控制VPC何时完成G1期,也控制VPC何时获得对细胞间模式信号作出反应并表达阴门命运的能力。