Chromatin Accessibility Shapes Growth and Stress Response in Blue Mold

Blue mold, caused by Penicillium expansum, is one of the most destructive postharvest diseases, leading to economic losses across fruit supply chains. Beyond rot, the fungus contaminates fruit-based products with patulin, raising food safety concerns. Previous research has revealed genomic features and certain transcription factors in P. expansum, yet the mechanisms controlling its gene expression remain poorly understood. Chromatin accessibility-the openness of DNA regions that allow transcription factor binding-plays a central role in gene regulation. However, its characterization in postharvest pathogens has been limited. Due to these challenges, there is a pressing need for deeper investigation into chromatin accessibility and transcriptional control in P. expansum.

A research team from Jiangsu University has published (DOI: 10.1093/hr/uhae264) a study in Horticulture Research (20 September 2024), unveiling the chromatin accessibility landscape of P. expansum and the role of the transcription factor PeAtf1. Using assay for transposase-accessible chromatin sequencing (ATAC-seq) and functional genetic analysis, the team mapped open chromatin regions during vegetative growth and apple infection, identifying key cis-regulatory elements and stress-related transcriptional responses. Their findings illuminate how this notorious pathogen adapts during infection and highlight PeAtf1 as a regulator of growth, reproduction, and stress tolerance.

By applying ATAC-seq, the researchers generated over 900 million sequence reads from P. expansum during vegetative growth and apple infection. They found a striking reduction in chromatin accessibility during infection, with peaks mainly concentrated in promoter regions, suggesting promoter-driven regulation dominates transcriptional activity. Motif analysis revealed six enriched cis-regulatory elements, many resembling known transcription factor binding sites from Saccharomyces cerevisiae.

The team then identified and knocked out PeAtf1, a basic leucine zipper (bZIP) transcription factor. Mutants lacking PeAtf1 showed severely impaired growth, reduced biomass, delayed spore germination, and diminished reproduction, though pathogenicity on apples remained unchanged. Stress assays revealed dual roles: PeAtf1 positively regulated tolerance to osmotic stress, but negatively affected responses to oxidative, membrane, and cell wall stresses. Interestingly, deletion of PeAtf1 upregulated oxidative stress response genes such as PeAP1, PeSOD, and PeCAT, enhancing fungal resilience to host-derived reactive oxygen species. This indicates a trade-off where growth and reproduction are weakened, yet stress tolerance is improved, maintaining virulence despite developmental defects.

Our study sheds light on how P. expansum orchestrates growth and stress adaptation at the chromatin level. By combining ATAC-seq with functional genetics, we discovered that PeAtf1 plays a dual role-promoting growth but suppressing certain stress responses. This paradox helps explain why mutants maintain pathogenicity even with impaired development. Understanding these regulatory networks is crucial for devising targeted control strategies that reduce fruit spoilage while limiting the risk of mycotoxin contamination in the global food supply".

Yiran Wang, lead author 

The findings provide a molecular framework for managing blue mold in postharvest fruit supply chains. By mapping chromatin accessibility and pinpointing PeAtf1 as a regulatory hub, the study identifies potential genetic or chemical targets to disrupt fungal growth or enhance fruit resistance. Insights into stress-response pathways could also inform the design of biocontrol agents or storage conditions that weaken the pathogen's survival strategies. Ultimately, these advances contribute to improving food safety, reducing economic losses from fruit decay, and developing sustainable postharvest management practices that benefit producers, distributors, and consumers alike.