Komoda, Y. | bioRxiv Science

bioRxiv2023

Fungal hacking of the plant sex-determination pathway via interference with AGL24 in Silene latifolia

Plants have evolved lineage-specific sex-determination systems that is determined not only by genetic factors, but also the surrounding environmental conditions, including interactions with pathogens. Silene latifolia is a model dioecious plant whose sexuality is genetically regulated by X/Y chromosomes; however, anther smut fungus mimics the plant Y chromosome and forcibly converts female plants to male. Here, transcriptome analyses of healthy or fungus-infected S. latifolia inflorescence meristems suggested that an orthologue of AGL24 (SlAGL24), a flowering activator, is a key factor in sex conversion via fungus infection. Overexpression of SlAGL24 in Arabidopsis thaliana suppressed stamen development, whereas knock-down of SlAGL24 in S. latifolia converted males into hermaphrodites. Furthermore, SlAGL24 expression affected sexual dimorphisms in S. latifolia. Our results propose an adaptive scenario wherein the anther smut fungus targets SlAGL24, as a master regulator connecting the fungal signal to sex determination, to confer male and potentially male-beneficial traits, effectively transmitting its teliospores.

plant biology↗

bioRxiv2018

USP15 participates in HCV propagation through the regulation of viral RNA translation and lipid droplet formation

Hepatitis C virus (HCV) utilizes cellular factors for an efficient propagation. Ubiquitin is covalently conjugated to the substrate to alter its stability or to modulate signal transduction. In this study, we examined the importance of ubiquitination for HCV propagation. We found that inhibition of de-ubiquitinating enzymes (DUBs) or overexpression of non-specific DUBs impaired HCV replication, suggesting that ubiquitination regulates HCV replication. To identify specific DUBs involved in HCV propagation, we set up an RNAi screening against DUBs and successfully identified ubiquitin-specific protease 15 (USP15) as a novel host factor for HCV propagation. Our studies showed that USP15 is involved in translation of HCV RNA and production of infectious HCV particles. In addition, deficiency of USP15 in human hepatic cell lines (Huh7 and Hep3B/miR122 cells) but not in a non-hepatic cell line (293T cells) impaired HCV propagation, suggesting that USP15 participates in HCV propagation through the regulation of hepatocyte-specific functions. Moreover, we showed that loss of USP15 had no effect on innate immune responses in vitro and in vivo. We also found that USP15-deficient Huh7 cells showed reductions in the sizes and numbers of lipid droplets (LDs), and addition of palmitic acids restored the production of infectious HCV particles. Taken together, these data suggest that USP15 participates in HCV propagation by regulating the translation of HCV RNA and formation of LDs.

microbiology↗