The study investigates the in vivo functions of the poorly understood Fam83f protein in zebrafish development and stress response. The key findings are:
Fam83f is strongly expressed in the embryonic hatching gland of developing zebrafish. Knockout of the fam83fa gene leads to premature hatching of the embryos, despite normal developmental rate.
Fam83fa knockout embryos show increased sensitivity to DNA-damaging agents like ionizing radiation and methyl methanesulfonate, but this is not due to altered p53 stability or activity.
Transcriptomic analysis reveals that loss of fam83fa leads to downregulation of genes encoding phosphatidylinositol-3-phosphate (PI(3)P) binding proteins, which are important for autophagy and lysosomal processes. This suggests Fam83f modulates autophagic/lysosomal pathways.
The Fam83fa protein itself is targeted to the lysosome when overexpressed, and this localization is dependent on a C-terminal signal sequence.
In summary, the zebrafish Fam83fa protein appears to play a key role in regulating autophagic/lysosomal processes, which in turn impacts embryonic hatching and the cellular response to DNA damage.
toiselle kielelle
lähdeaineistosta
biorxiv.org
Tärkeimmät oivallukset
by Jones,R. A.,... klo www.biorxiv.org 02-12-2024
https://www.biorxiv.org/content/10.1101/2024.02.10.579757v1Syvällisempiä Kysymyksiä