The C-elegans hunchback homolog, hbl-1, controls temporal patterning and is a probable microRNA target
The C-elegans hunchback homolog, hbl-1, controls temporal patterning and is a probable microRNA target
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DOI：
10.1016/s1534-5807(03)00124-2
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发表时间：
2003-05-01
影响因子：
11.8
通讯作者：
Slack, FJ
中科院分区：
文献类型：
--
作者：
Lin, SY;Johnson, SM;Slack, FJ
Hunchback调节果蝇神经母细胞的时间特性。在这里，我们表明hbl-1，C. elegans hunchback直系同源物，也控制时间模式。此外，hbl-1可能是通过其3 'UTR调控microRNA的靶标。HBL-1功能丧失导致成体缝细胞命运的早熟表达。这种表型类似于lin-41的功能丧失，lin-41是let-7 microRNA的已知靶标。像lin-41突变一样，hbl-1功能丧失部分抑制let-7突变。hbl-1 3 'UTR对于在发育过程中下调报告基因是必需的且足够的，并且let-7和lin-4 microRNA对于HBL-1/GFP下调都是必需的。hbl-1 3 'UTR中的多个元件显示与调节性microRNA互补，表明microRNA直接控制hbl-1。microRNA同样可以在神经系统的时间模式化过程中调节Drusophila hunchback。
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.