Abstract
Programmed cell death occurs in a highly reproducible manner during Caenorhabditis elegans development. We demonstrate that, during embryogenesis, miR-35 and miR-58 bantam family microRNAs (miRNAs) cooperate to prevent the precocious death of mothers of cells programmed to die by repressing the gene egl-1, which encodes a proapoptotic BH3-only protein. In addition, we present evidence that repression of egl-1 is dependent on binding sites for miR-35 and miR-58 family miRNAs within the egl-1 3' untranslated region (UTR), which affect bothmRNA copy number and translation. Furthermore, using single-molecule RNA fluorescent in situ hybridization (smRNA FISH), we show that egl-1 is transcribed in the mother of a cell programmed to die and that miR-35 and miR-58 family miRNAs prevent this mother from dying by keeping the copy number of egl-1 mRNA below a critical threshold. Finally, miR-35 and miR-58 family miRNAs can also dampen the transcriptional boost of egl-1 that occurs specifically in a daughter cell that is programmed to die. We propose that miRNAs compensate for lineagespecific differences in egl-1 transcriptional activation, thus ensuring that EGL-1 activity reaches the threshold necessary to trigger death only in daughter cells that are programmed to die.
Item Type: | Journal article |
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Faculties: | Biology > Department Biology II |
Research Centers: | Center for Integrated Protein Science Munich (CIPSM) |
Subjects: | 500 Science > 540 Chemistry 500 Science > 570 Life sciences; biology |
URN: | urn:nbn:de:bvb:19-epub-55986-2 |
ISSN: | 0890-9369 |
Language: | English |
Item ID: | 55986 |
Date Deposited: | 14. Jun 2018, 10:01 |
Last Modified: | 04. Nov 2020, 13:36 |