Autophagy is an evolutionarily conserved process that recycles damaged or unwanted cellular components, and has been linked to plant immunity. However, how autophagy contributes to plant immunity is unknown. Here we reported that the plant autophagic machinery targets the virulence factor βC1 of Cotton leaf curl Multan virus (CLCuMuV) for degradation through its interaction with the key autophagy protein ATG8. A V32A mutation in βC1 abolished its interaction with NbATG8f, and virus carrying βC1^V32A showed increased symptoms and viral DNA accumulation in plants. Furthermore, silencing of autophagy-related genes ATG5 and ATG7 reduced plant resistance to the DNA viruses CLCuMuV, Tomato yellow leaf curl virus, and Tomato yellow leaf curl China virus, whereas activating autophagy by silencing GAPC genes enhanced plant resistance to viral infection. Thus, autophagy represents a novel anti-pathogenic mechanism that plays an important role in antiviral immunity in plants.

Gene silencing is a natural antiviral defense mechanism in plants. For effective infection, plant viruses encode viral silencing suppressors to counter this plant antiviral response. The geminivirus-encoded C4 protein has been identified as a gene silencing suppressor, but the underlying mechanism of action has not been characterized. Here, we report that Cotton Leaf Curl Multan virus (CLCuMuV) C4 protein interacts with S-adenosyl methionine synthetase (SAMS), a core enzyme in the methyl cycle, and inhibits SAMS enzymatic activity. By contrast, an R13A mutation in C4 abolished its capacity to interact with SAMS and to suppress SAMS enzymatic activity. Overexpression of wild-type C4, but not mutant C4^R13A, suppresses both transcriptional gene silencing (TGS) and post-transcriptional gene silencing (PTGS). Plants infected with CLCuMuV carrying C4^R13A show decreased levels of symptoms and viral DNA accumulation associated with enhanced viral DNA methylation. Furthermore, silencing of NbSAMS2 reduces both TGS and PTGS, but enhanced plant susceptibility to two geminiviruses CLCuMuV and Tomato yellow leaf curl China virus. These data suggest that CLCuMuV C4 suppresses both TGS and PTGS by inhibiting SAMS activity to enhance CLCuMuV infection in plants. Geminiviruses are single-stranded DNA (ssDNA) viruses that infect a wide range of plant species and are responsible for substantial crop damage worldwide. However, how geminiviruses inhibit plant antiviral gene silencing defense is unclear. Here, we report that a single geminiviral protein CLCuMuV C4 inhibits both plant transcriptional gene silencing (TGS) and post-transcriptional gene silencing (PTGS) to promote an effective viral infection. We show that CLCuMuV C4 protein interacts with SAMS, a core enzyme in methyl cycle, and inhibits SAMS activity. Overexpression of CLCuMuV C4 reduces the DNA methylation levels of both a transgene and an endogenous locus. Further, silencing of SAMS reduced both TGS and PTGS, and enhanced viral infection while CLCuMuV virus carrying a mutation in C4 that fails to interact with SAMS showed decreased infection. These findings reveal a novel mechanism by which the CLCuMuV C4 protein suppress SAMS mediated TGS and PTGS, leading to enhanced viral infection in plant.

Autophagy plays an important role in plant–pathogen interactions. Several pathogens including viruses induce autophagy in plants, but the underpinning mechanism remains largely unclear. Furthermore, in virus–plant interactions, viral factor(s) that induce autophagy have yet to be identified. Here, we report that the βC1 protein of Cotton leaf curl Multan betasatellite (CLCuMuB) interacts with cytosolic glyceraldehyde-3-phosphate dehydrogenase (GAPC), a negative autophagic regulator, to induce autophagy in Nicotiana benthamiana. CLCuMuB βC1 bound to GAPCs and disrupted the interaction between GAPCs and autophagy-related protein 3 (ATG3). A mutant βC1 protein (βC13A) in which I45, Y48, and I53 were all substituted with Ala (A), had a dramatically reduced binding capacity with GAPCs, failed to disrupt the GAPCs-ATG3 interactions and failed to induce autophagy. Furthermore, mutant virus carrying βC13A showed increased symptoms and viral DNA accumulation associated with decreased autophagy in plants. These results suggest that CLCuMuB βC1 activates autophagy by disrupting GAPCs–ATG3 interactions.

Plants may experience adverse effects from Cadmium (Cd). As a result of its toxicity and mobility within the soil-plant continuum, it is attracting the attention of soil scientists and plant nutritionists. In this study, we subjected young Eruca sativa Mill. seedlings to different levels of Cd applications (0, 1.5, 6 and 30 µmol/L) via pot experiment to explore its morpho-physio-biochemical adaptations. Our results revealed a significant Cd accumulation in leaves at high Cd stress. It was also demonstrated that Cd stress inhibited photosynthetic rate and pigment levels, ascorbate peroxidase (APX), guaiacol peroxidase (GPX), catalase (CAT), and superoxide dismutase (SOD) enzyme activities, and increased malondialdehyde (MDA) levels. Conversely, the concentration of total ascorbate (TAS) increased at all levels of Cd application, whereas that of ascorbic acid (ASA), and dehydroascorbate (DHA) increased at 1.5 (non-significant), 6, 30 and 6 µmol/L (significant), though their concentrations decreased non-significantly at 30 µmol/L application. In conclusion, Cd-subjected E. sativa seedlings diverted much energy from growth towards the synthesis of anti-oxidant metabolites and osmolytes. However, they did not seem to have protected the E. sativa seedlings from Cd-induced oxidative stress, causing a decrease in osmotic adjustment, and an increase in oxidative damage, which resulted in a reduction in photosynthesis and growth. Accordingly, we recommend that the cultivation of E. sativa should be avoided on soil with Cd contamination.

It has been shown that jasmonic acid (JA) can alleviate drought stress. Nevertheless, there are still many questions regarding the JA-induced physiological and biochemical mechanisms that underlie the adaptation of plants to drought stress. Hence, the aim of this study was to investigate whether JA application was beneficial for the antioxidant activity, plant performance, and growth of Grewia asiatica L. Therefore, a study was conducted on G. asiatica plants aged six months, exposing them to 100% and 60% of their field capacity. A JA application was only made when the plants were experiencing moderate drought stress (average stem water potential of 1.0 MPa, considered moderate drought stress), and physiological and biochemical measures were monitored throughout the 14-day period. In contrast to untreated plants, the JA-treated plants displayed an improvement in plant growth by 15.5% and increased CO₂ assimilation (AN) by 43.9% as well as stomatal conductance (GS) by 42.7% on day 3. The ascorbate peroxidase (APX), glutathione peroxidase (GPX), and superoxide dismutase (SOD) activities of drought-stressed JA-treated plants increased by 87%, 78%, and 60%, respectively, on day 3. In addition, G. asiatica plants stressed by drought accumulated 34% more phenolics and 63% more antioxidants when exposed to JA. This study aimed to understand the mechanism by which G. asiatica survives in drought conditions by utilizing the JA system.

Chitinases are responsible for catalyzing the hydrolysis of chitin and contribute to plant defense against fungal pathogens by degrading fungal chitin. In this study, genome-wide identification of the chitinase gene family of wild apple (Malus sieversii) and domesticated apple (Malus domestica) was conducted, and the expression profile was analyzed in response to Valsa mali infection. A total of 36 and 47 chitinase genes belonging to the glycosyl hydrolase 18 (GH18) and 19 (GH19) families were identified in the genomes of M. sieversii and M. domestica, respectively. These genes were classified into five classes based on their phylogenetic relationships and conserved catalytic domains. The genes were randomly distributed on the chromosomes and exhibited expansion by tandem and segmental duplication. Eight of the 36 MsChi genes and 17 of the 47 MdChi genes were differentially expressed in response to V. mali inoculation. In particular, MsChi35 and its ortholog MdChi41, a class IV chitinase, were constitutively expressed at high levels in M. sieversii and domesticated apple, respectively, and may play a crucial role in the defense response against V. mali. These results improve knowledge of the chitinase gene family in apple species and provide a foundation for further studies of fungal disease prevention in apple.