biostudies-literatureIlbay ONational Institutes of HealthNIGMS NIH HHSdev183111https://www.ebi.ac.uk/biostudies/studies/S-EPMC6857590biostudies-literatureUnknown146(21)MicroRNAs target complementary mRNAs for degradation or translational repression, reducing or preventing protein synthesis. In <i>Caenorhabditis elegans</i>, the transcription factor HBL-1 (Hunchback-like 1) promotes early larval (L2)-stage cell fates, and the <i>let-7</i> family microRNAs temporally downregulate HBL-1 to enable the L2-to-L3 cell-fate progression. In parallel to <i>let-7</i>-family microRNAs, the conserved RNA-binding protein LIN-28 and its downstream gene <i>lin-46</i> also act upstream of HBL-1 in regulating the L2-to-L3 cell-fate progression. The molecular function of LIN-46, and how the <i>lin-28-lin-46</i> pathway regulates HBL-1, are not understood. Here, we report that the regulation of HBL-1 by the <i>lin-28-lin-46</i> pathway is independent of the <i>let-7</i>/<i>Development (Cambridge, England)Regulation of nuclear-cytoplasmic partitioning by the <i>lin-28</i>-<i>lin-46</i> pathway reinforces microRNA repression of HBL-1 to confer robust cell-fate progression in <i>C. elegans</i>.PMC6857590R01GM088365R01 GM088365R35 GM131741R01 GM034028Ilbay OAmbros VfalseRegulation of nuclear-cytoplasmic partitioning by the <i>lin-28</i>-<i>lin-46</i> pathway reinforces microRNA repression of HBL-1 to confer robust cell-fate progression in <i>C. elegans</i>.MicroRNAs target complementary mRNAs for degradation or translational repression, reducing or preventing protein synthesis. In <i>Caenorhabditis elegans</i>, the transcription factor HBL-1 (Hunchback-like 1) promotes early larval (L2)-stage cell fates, and the <i>let-7</i> family microRNAs temporally downregulate HBL-1 to enable the L2-to-L3 cell-fate progression. In parallel to <i>let-7</i>-family microRNAs, the conserved RNA-binding protein LIN-28 and its downstream gene <i>lin-46</i> also act upstream of HBL-1 in regulating the L2-to-L3 cell-fate progression. The molecular function of LIN-46, and how the <i>lin-28-lin-46</i> pathway regulates HBL-1, are not understood. Here, we report that the regulation of HBL-1 by the <i>lin-28-lin-46</i> pathway is independent of the <i>let-7</i>/<i>2019-01-01T00:00:00Z2019 Nov2025-04-04T11:52:35.117Z2020-11-03T08:02:46ZS-EPMC68575903159765810.1242/dev.183111