Saikia, R. | Search bioRxiv

bioRxiv2024

Identification of a novel begomovirus betasatellite and occurrence of a viral complex associated with leaf curl disease in Bhut Jolokia in Assam

Bhut Jolokia (Capsicum chinense Jacq.) is one of the hottest chillies and an economically important crop in the northeastern regions of India. A major problem in the cultivation of Bhut Jolokia is the occurrence of leaf curl disease, which causes huge annual economic losses. The present study reveals the viral complex associated with the leaf curl disease in Bhut Jolokia collected from different geographical locations in Assam. A novel begomovirus betasatellite component was identified in two Bhut Jolokia samples, which was phylogenetically distinct from known begomovirus betasatellites. DAS-ELISA and PCR analysis confirmed the presence of multiple plant viruses including Chilli leaf curl virus (ChiLCV), Cucumber mosaic virus (CMV), Potato virus Y (PVY) and Tomato leaf curl virus (ToLCV) in most of the naturally infected Bhut Jolokia samples. Phylogenetic analysis revealed that the coat protein (CP) gene of ChiLCVs and ToLCVs were highly conserved compared to the CP of CMV.

molecular biology↗

bioRxiv2021

Nup358 regulates remodelling of ER-mitochondrial contact sites and autophagy

The contact sites between ER and mitochondria regulate several cellular processes including inter-organelle lipid transport, calcium homeostasis and autophagy. However, the mechanisms that regulate the dynamics and functions of these contact sites remain unresolved. We show that annulate lamellae (AL), a relatively unexplored subcellular structure representing subdomains of ER enriched with a subset of nucleoporins, are present at ER-mitochondria contact sites (ERMCS). Depletion of one of the AL-resident nucleoporins, Nup358, results in increased contacts between ER and mitochondria. Mechanistically, Nup358 modulates ERMCS dynamics by restricting mTORC2/Akt signalling. Our results suggest that growth factor-mediated remodelling of ERMCS depends on a reciprocal binding of Nup358 and mTOR to the ERMCS tethering complex consisting of VAPB and PTPIP51. Furthermore, Nup358 also interacts with IP3R, an ERMCS-enriched Ca2+ channel, and controls Ca2+ release from the ER. Consequently, depletion of Nup358 leads to elevated cytoplasmic Ca2+ and autophagy via activation of Ca2+/CaMKK2/AMPK axis. Our study thus uncovers a novel role for AL, particularly for Nup358, in regulating mTORC2-mediated ERMCS remodelling and Ca2+-directed autophagy, possibly via independent mechanisms.

cell biology↗