Tissue-specific requirement of Polr1D in the prothoracic gland for ecdysone-mediated developmental transitions in Drosophila melanogaster.

Abstract

Background: POLR1D is a shared subunit of RNA Polymerases I and III, which transcribe the rRNA incorporated into ribosomes. Mutations in POLR1D cause Treacher Collins syndrome, a craniofacial disorder that arises from impaired ribosome biogenesis in neural crest cells. Previously, we found that RNAi knockdown of Polr1D in several non-neural Drosophila tissues caused developmental defects that phenocopy mutations affecting ecdysone signaling. Ecdysone is a steroid hormone produced in the prothoracic gland (PG) of insects that triggers developmental transitions. Here, we show that Polr1D is required for PG development and ecdysone production to facilitate larval developmental transitions.

Results: We found that Polr1D RNAi in the PG causes larval developmental arrest due to defective peripheral ecdysone signaling. We also found that Polr1D is required for the growth of PG cells and for maintaining nucleolar structure. We found that Polr1D is required for the synthesis of mature ribosomes and the production of the Pol III-transcribed 7SK RNA. Furthermore, developmental arrest of Polr1D RNAi larvae and Polr1D mutant (G30R) larvae was partially rescued by treatment with exogenous ecdysone.

Conclusion: These results demonstrate a role for Drosophila Polr1D in PG development and suggest that disruptions in human Polr1D might impact additional cell types during development.