Moss E G, Lee R C, Ambros V
Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755, USA.
Cell. 1997 Mar 7;88(5):637-46. doi: 10.1016/s0092-8674(00)81906-6.
Mutations in the heterochronic gene lin-28 of C. elegans cause precocious development where diverse events specific to the second larval stage are skipped. lin-28 encodes a cytoplasmic protein with a cold shock domain and retroviral-type (CCHC) zinc finger motifs, consistent with a role for LIN-28 in posttranscriptional regulation. The 3'UTR of lin-28 contains a conserved element that is complementary to the 22 nt regulatory RNA product of lin-4 and that resembles seven such elements in the 3'UTR of the heterochronic gene lin-14. Both lin-4 activity and the lin-4-complementary element (LCE) are necessary for stage-specific regulation of lin-28. Deleting the LCE produces a dominant gain-of-function allele that causes a retarded phenotype, indicating that lin-28 activity is a switch that controls choices of stage-specific fates.
秀丽隐杆线虫异时性基因lin-28的突变会导致发育早熟，即跳过第二幼虫阶段特有的各种事件。lin-28编码一种具有冷休克结构域和逆转录病毒型（CCHC）锌指基序的细胞质蛋白，这与LIN-28在转录后调控中的作用一致。lin-28的3'非翻译区包含一个保守元件，该元件与lin-4的22个核苷酸调控RNA产物互补，并且类似于异时性基因lin-14的3'非翻译区中的七个这样的元件。lin-4活性和lin-4互补元件（LCE）对于lin-28的阶段特异性调控都是必需的。删除LCE会产生一个显性功能获得等位基因，导致发育迟缓的表型，表明lin-28活性是一个控制阶段特异性命运选择的开关。
