The multiple lncRNAs encodinghsrωgene is essential for oogenesis inDrosophila

Abstract

AbstractTo understand low viability and fecundity associated with perturbed levels of developmentally expressed and stress-induciblehsrωlncRNAs, we examined oogenesis in near-nullhsrω66homozygotes, and following targeted down- or up-regulation ofhsrωtranscripts in developing egg chambers. Short lifespan and poor fecundity,hsrω66females 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 ofhsrωtranscripts, and oogenesis regulators like Notch, Cut, Caz/dFus and TBPH/TDP-43 on oogenesis were also examined. While alteredhsrωtranscript 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 andhsrωlncRNA levels were not evident. Ecdysone feeding tohsrω66females or targeted expression of thehsrω-RHtranscripts inhsrω66egg chamber substantially restored normal oogenesis. Misexpression ofhsrωlncRNAs thus adversely affects oogenesis through disruption of intra- and inter-organ signaling.