lnc5714 participates in silkworm resistance to Nosema bombycis infection by regulating MRPL4-related host energy metabolism.

Abstract

Pebrine caused by Nosema bombycis is a devastating infectious disease that severely constrains the development of the sericulture industry. Because this pathogen is highly dependent on host-derived energy and nutrients, identifying key factors that regulate host metabolism is crucial for elucidating the mechanisms of disease resistance. In this study, we identified and cloned a long non-coding RNA, lnc5714, that was differentially induced in response to N. bombycis infection. Subcellular localization analysis showed that lnc5714 was predominantly distributed in the cytoplasm. Functional assays demonstrated that overexpression of lnc5714 significantly inhibited the replication of N. bombycis, whereas knockdown of lnc5714 promoted its proliferation, confirming that lnc5714 is a resistance-associated factor. Network prediction and experimental validation further revealed that the potential target gene of lnc5714 is the mitochondrial ribosomal protein BmMRPL4. Further analyses confirmed that the expression of BmMRPL4 was negatively regulated by lnc5714, and that the expression level of BmMRPL4 directly affected intracellular ATP levels: overexpression of BmMRPL4 increased ATP content and promoted pathogen proliferation, whereas its knockdown produced the opposite effect. Taken together, our findings demonstrate that lnc5714 suppresses the expression of BmMRPL4 by downregulating its mRNA level, thereby weakening mitochondrial energy output in host cells and restricting the replication of N. bombycis. This study provides a new theoretical basis for the identification of disease-resistance molecular markers and the genetic improvement of silkworms.