| dc.description.abstract |
The serine hydrolase (SH) superfamily is one of the largest enzyme classes across species, with diverse functions ranging from immunity to metabolism to development. Like other metazoans, early development in Drosophila is primarily regulated by maternally deposited gene products, including mRNAs and proteins. Studies over several decades have demonstrated critical roles for maternally deposited SHs in dorsoventral patterning and immune responses. Despite this knowledge, a significant majority of SH genes (84%) remain functionally uncharacterized, and a substantial number of these genes (136 out of 354) are maternally deposited. Here, we explore the maternal role(s) of one such maternally deposited but functionally uncharacterized metabolic SH, CG11309. Loss of CG11309 leads to partial embryonic lethality (~50%), correlated with aberrant centrosome behaviour and defects in nuclear cycles, which are observable from early embryonic stages. Moreover, mutant embryos show a reduced number of primordial germ cells (PGCs), the precursors of gametes in adults. We observe that the reduction in PGC count in blastoderm CG11309 null embryos is associated with defective pole cell budding and irregular vasa sequestration around the nuclei in the earlier stages. Consistently, we observe aberrant localization of components of the contractile ring, essential for bud extrusion from the embryo to form PGCs. We present a detailed analysis of CG11309 to understand its novel roles during early development, along with a systematic approach to generating new reagents for future investigations. |
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