ArticleNature communications2025
A fungal effector promotes infection via stabilizing a negative regulatory factor of chloroplast immunity.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Functional Characterization of Two Adjacent Oxygenase Genes,Journal of fungi (Basel, Switzerland) · 2026Article
- Securing the replication ground: how barley stripe mosaic virus safeguards the host chloroplast envelope.The Plant cell · 2026Article
- The DENN Protein SMD1 Forms a Signalling Hub With Rab GTPase YPT1 to Regulate Diverse Biological Processes in Phytopathogenic Fungi and Serves as a HIGS Target for Crop Protection.Molecular plant pathology · 2026Article
- Transcriptomic profiling of wheat (Frontiers in plant science · 2026Article
- Study on a temperature-dependent selective soil treatment agent in regulating tobacco rhizosphere microbial community and controlling root and stem diseases.Frontiers in microbiology · 2026Article
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Authors and funding
14 authors.
Funding
Abstract
Chloroplasts are crucial players in immunity and photosynthesis. However, how chloroplasts arrange the transition between photosynthesis and immunity and how pathogens manipulate this transition remains elusive. Here we report an effector SsCm1 from Sclerotinia sclerotiorum, one of devastating phytopathogenic fungi, inhibits chloroplast immunity and resistance to pathogens, and alleviates photoinhibition in immune state. This is accomplished through stabilizing the conserved chloroplast protein MORF2, which is degraded during immunization and is a suppressor of photoinhibition, cell death, and chloroplast immunity. Overexpression of SsCm1 or MORF2 in plants represses basic immunity and resistance to pathogens, whereas deletion of SsCm1 reduces S. sclerotiorum virulence. Notably, SsCm1 possesses no chorismate mutase activity, which is different from the previously reported Cm effectors. This work reveals a strategy to fine-tune growth-defense balance in chloroplasts by manipulating MORF2, and a pathogenic strategy to subvert the process and promote infection via enzymatically nonfunctional effector stabilizing MORF2.
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