PdEch1 regulates the conidia production of Penicillium digitatum and oxidative stress tolerance

Citrus is the most widely cultivated fruit crop with the highest yield worldwide, and postharvest losses caused by Penicillium digitatum account for 90% of the total postharvest losses in citrus. Enoyl-CoA hydratase (ECH) catalyzes the second step of β-oxidation, the primary pathway of fatty acid catabolism. Previous studies have shown that ECH deficiency causes developmental delay, mitochondrial dysfunction, nervous system damage and other symptoms, and these phenotypes have been reported in humans, mice and Drosophila.

This study aimed to characterize the biological function of the PdEch1 gene in P. digitatum.

The PdEch1 gene deletion strain ΔPdEch1 and complemented strain ΔPdEch1-C were constructed via Agrobacterium-mediated genetic transformation. Physiological assays were performed, including mycelial growth rate measurement, conidial yield quantification, conidial germination rate assay, stress agent sensitivity testing, and pathogenicity evaluation. In addition, transcriptome sequencing and quantitative real-time PCR (qRT-PCR) were conducted.

Deletion of PdEch1 increased conidial production by 51.4% and altered the expression of conidiation-related genes such as brlA and rodA. Furthermore, the ΔPdEch1 strain exhibited significantly enhanced resistance to H₂O₂. Compared with the wild-type strain N1, mycelial growth, conidial germination, and pathogenicity of P. digitatum were not affected.

This study reveals that the PdEch1 gene is closely associated with conidial formation and oxidative stress tolerance in P. digitatum, providing a reference for the development and screening of target sites for novel fungicides.