Disrupting PEX16 and PEX14 reveals distinct roles in female reproductive capacity and lifespan, suggesting important mechanistic differences.
Peroxisomes are essential for the metabolism of very long-chain fatty acids (VLCFAs). Their biogenesis requires peroxins encoded by the PEX genes. While the significance of PEX14 has been established in the major rice pest the brown planthopper (Nilaparvata lugens), the role of PEX16 as a peroxisome biogenesis initiator remains uncharacterized in this pest. This study aimed to elucidate the functional importance of N. lugens PEX16 (NlPEX16) by comparing the impacts of disrupting NlPEX16 and NlPEX14. NlPEX16 encodes a conserved membrane protein localized to peroxisomes. NlPEX16 silencing recapitulated the key phenotypic features of NlPEX14 deficiency, including reduced female lifespan, disrupted ovarian development, and severely impaired oviposition capacity in N. lugens. NlPEX16 knockdown accelerated female mortality kinetics and worsened fecundity more profoundly than NlPEX14 knockdown, despite modest VLCFA accumulation. Crucially, vitellogenin protein expression remained unchanged in NlPEX16-depleted females, in contrast with the 95% down-regulation observed in NlPEX14-impaired females. Furthermore, NlPEX16 silencing did not affect NlPEX14 protein expression. Similar to NlPEX14, NlPEX16 is essential for the survival and fecundity of the female brown planthopper. However, the mechanisms underlying the shared phenotypic outcomes are different. The non-redundant functions of NlPEX16 and NlPEX14 highlight how peroxisomal proteins orchestrate physiology through distinct yet interconnected mechanisms.
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Liu et al. (2025) studied this question.
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