The multiple lncRNAs encodinghsrω gene is essential for oogenesis inDrosophila

Abstract

To understand low viability and fecundity associated with perturbed levels of developmentally expressed and stress-inducible hsrω lncRNAs, we examined oogenesis in near-null hsrω66 homozygotes, and following targeted down- or up-regulation of hsrω transcripts in developing egg chambers. Short lifespan and poor fecundity, hsrω66 females showed fewer ovarioles, reduced Vasa and weak fusomes in early cysts, high apoptosis and poor actin nuclear-cage in mid-stage chambers, low Cut levels in late chambers and ovulation block. Effects of co-alterations in levels of hsrω transcripts, and oogenesis regulators like Notch, Cut, Caz/dFus and TBPH/TDP-43 on oogenesis were also examined. While altered hsrω transcript levels did not modulate defects following active Notch overexpression in follicle cells, they varyingly enhanced or suppressed defects due to targeted down- or up-regulation of Cut, Caz/dFus or TBPH/TDP-43. As expected of a gene producing multiple lncRNAs that interact with diverse regulatory molecules, simple linear causal inter-relations between oogenesis regulators and hsrω lncRNA levels were not evident. Ecdysone feeding to hsrω66 females or targeted expression of the hsrω-RH transcripts in hsrω66 egg chamber substantially restored normal oogenesis. Misexpression of hsrω lncRNAs thus adversely affects oogenesis through disruption of intra- and inter-organ signaling.