Yellow mosaic disease (YMD), incited by mungbean yellow mosaic virus (MYMV), is a primary viral disease that reduces mungbean production in South Asia, especially in India. There is no detailed knowledge regarding the genes and molecular mechanisms conferring resistance of mungbean to MYMV. Therefore, disclosing the genetic and molecular bases related to MYMV resistance helps to develop the mungbean genotypes with MYMV resistance. In this study, transcriptomes of mungbean genotypes, VGGRU-1 (resistant) and VRM (Gg) 1 (susceptible) infected with MYMV were compared to those of uninfected controls. The number of differentially expressed genes (DEGs) in the resistant and susceptible genotypes was 896 and 506, respectively. Among them, 275 DEGs were common between the resistant and susceptible genotypes. Functional annotation of DEGs revealed that the DEGs belonged to the following categories defense and pathogenesis, receptor-like kinases; serine/threonine protein kinases, hormone signaling, transcription factors, and chaperons, and secondary metabolites. Further, we have confirmed the expression pattern of several DEGs by quantitative real-time PCR (qRT-PCR) analysis. Collectively, the information obtained in this study unveils the new insights into characterizing the MYMV resistance and paved the way for breeding MYMV resistant mungbean in the future.

Ferroptosis remains an underexamined iron- and lipid peroxides-driven cell death modality despite its importance to several human and plant diseases and to immunity thereof. Here, we utilized chemical cell biology, molecular genetics and biochemical analyses to gain insights into how the fungal pathogen Magnaporthe oryzae undergoes ferroptosis strictly in the spore cells to successfully transit to infectious development. We reveal a complex functional interdependency and crosstalk between intrinsic ferroptosis and autophagy-mediated mitochondrial degradation. Mechanistically, the requirement of mitophagy for ferroptotic cell death was attributed to its ability to maintain a pool of metabolically active mitochondria. Pharmacological disruption of the electron transport chain or membrane potential led to complete inhibition of ferroptosis, thus simulating the loss of mitophagy phenotypes. Conversely, increased mitochondrial membrane potential in a mitophagy-defective mutant alleviated the ferroptosis defects therein. Graded inhibition of mitochondrial coenzyme Q biosynthesis with or without ferroptosis inhibitor liproxstatin-1 distinguished its antioxidant function in such regulated cell death. Membrane potential-dependent regulation of ATP synthesis and iron homeostasis, as well as dynamics of tricarboxylic acid cycle enzyme AcoA (aconitase A) in the presence or absence of mitophagy, mitochondrial poisoning or iron chelation further linked mitochondrial metabolism to ferroptosis. Last, we present an important bioenergetics- and redox-based mitochondrial regulon essential for intrinsic ferroptosis and its precise role in fungal pathogenesis leading up to the establishment of the devastating rice blast disease.