| 41104 |
Q9VHG4 |
RENR_DROME |
ATPase H(+)-transporting accessory protein 2 (Renin homolog receptor) (dPRR) [Cleaved into: ATPase H(+)-transporting accessory protein 2 N-terminal fragment; ATPase H(+)-transporting accessory protein 2 C-terminal fragment] |
DISRUPTION PHENOTYPE |
RNAi-mediated knockdown is lethal (PubMed:20579883). RNAi-mediated knockdown in the wings results in increased apoptosis, endoplasmic reticulum stress and lipid accumulation (PubMed:20579883, PubMed:20579879, PubMed:29127204, PubMed:29995586). This is accompanied by severe growth defects including venation defects, defective wing-hair polarity (as a result of defective fz and stan trafficking) and wg signaling (PubMed:20579883, PubMed:20579879, PubMed:29127204, PubMed:29995586). RNAi-mediated knockdown in the notum causes severe planar polarity defects affecting orientation morphology and number of sensory bristles or microchaetae (PubMed:20579879). RNAi-mediated knockdown in the eye results in defective phototaxis and presynaptic transmission in vacuolated photoreceptor neurons and pigment cells (PubMed:26376863). RNAi-mediated knockdown in neurons leads to defective autophagy and neurodegeneration, impaired synapse morphology, ultrastructural organization and axonal transport of the active zone component brp, ultimately resulting in lethality at different developmental stages (PubMed:26376863). The few adult survivors show strongly reduced spontaneous movements and poor climbing abilities (PubMed:26376863). RNAi-mediated knockdown in the mushroom body results in altered short- and long-term memory (PubMed:26376863). RNAi-mediated knockdown in the fat body results in increased autophagy (PubMed:29127204). {ECO:0000269|PubMed:20579879, ECO:0000269|PubMed:20579883, ECO:0000269|PubMed:26376863, ECO:0000269|PubMed:29127204, ECO:0000269|PubMed:29995586}. |