The C-elegans hunchback homolog, hbl-1, controls temporal patterning and is a probable microRNA target

被引:274
作者
Lin, SY
Johnson, SM
Abraham, M
Vella, MC
Pasquinelli, A
Gamberi, C
Gottlieb, E
Slack, FJ
机构
[1] Yale Univ, Dept Mol Cellular & Dev Biol, New Haven, CT 06520 USA
[2] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA
[3] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02114 USA
[4] Univ Texas, Inst Cell & Mol Biol, Austin, TX 78712 USA
关键词
D O I
10.1016/S1534-5807(03)00124-2
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Hunchback regulates the temporal identity of neuroblasts in Drosophila. Here we show that hbl-1, the C. elegans hunchback ortholog, also controls temporal patterning. Furthermore, hbl-1 is a probable target of microRNA regulation through its 3'UTR. hbl-1 loss-of-function causes the precocious expression of adult seam cell fates. This phenotype is similar to loss-of-function of lin-41, a known target of the let-7 microRNA. Like lin-41 mutations, hbl-1 loss-of-function partially suppresses a let-7 mutation. The hbl-1 3'UTR is both necessary and sufficient to downregulate a reporter gene during development, and the let-7 and lin-4 microRNAs are both required for HBL-1/GFP downregulation. Multiple elements in the hbl-1 3'UTR show complementarity to regulatory microRNAs, suggesting that microRNAs directly control hbl-1. MicroRNAs may likewise function to regulate Drusophila hunchback during temporal patterning of the nervous system.
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收藏
页码:639 / 650
页数:12
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