• MCA delayed CGM development and softening in P. digitatum-infected navel oranges. • MCA decreased activities of CWDEs and maintained cell wall integrity. • Enhanced resistance to CGM may be linked to ERF017/109, DREB1D, MYB108, and WRKY75. • Our study unveiled a sustainable postharvest antifungal for citrus preservation. The regulatory mechanisms through which trans -4-methoxycinnamaldehyde (MCA) treatment inhibited the development of fungal diseases in postharvest citrus fruits, particularly the widespread occurrence of citrus green mold (CGM) caused by Penicillium digitatum , remained inadequately understood. Herein, 0.4 g/L MCA treatment was found to effectively slow the progression of P. digitatum infection and reduce the severity of CGM in harvested navel orange, and many physiological traits were measured, including fruit firmness, electrolyte leakage, malondialdehyde level, and cell wall polysaccharides (pectin, water-soluble pectin, cellulose, and hemicellulose) contents, as well as cell wall-degrading enzymes activities and their encoding genes expression. The transcriptomic sequencing data revealed that MCA treatment significantly diminished the number of DEGs in fruits infected with P. digitatum when compared to healthy fruits. A total of 432 DEGs were identified among the three groups, including 42 DEGs associated with cell wall degradation and 29 TFs related to CGM resistance. Real-time PCR investigations verified that the expression levels of CsPME3, CsPG2, CsCLE1, CsXTH9 , and most of the 10 TFs were up-regulated by MCA treatment, whereas the expression levels of CsGal6, CsMYB51 , and CsWRKY7 were suppressed during the later stages of P. digitatum infection. Thus, our results collectively proved that these genes responsive to MCA may play crucial roles in maintaining cell wall integrity to enhance fruit resistance to CGM, suggesting that MCA treatment could represent a promising strategy for preventing postharvest fungal diseases in citrus fruits.
Huang et al. (Wed,) studied this question.