Abstract

Apple replant disease (ARD) has led to severe yield and quality reduction in the apple industry. Fusarium solani (F. solani) has been identified as one of the main microbial pathogens responsible for ARD. Auxin (indole-3-acetic acid, IAA), as an endogenous hormone in plants, is involved in almost all plant growth and development processes and plays a role in plant immunity against pathogens. Gretchen Hagen3 (GH3) is one of the early/primary auxin response genes. The aim of this study was to evaluate the function of MdGH3-2 and MdGH3-12 in the defense response of F. solani by treating MdGH3-2/12 RNAi plants with F. solani. These results show that under F. solani infection, RNAi of MdGH3-2/12 inhibited plant biomass accumulation and aggravated root damage. After inoculation of F. solani, MdGH3-2/12 RNAi inhibited the biosynthesis of acid-amido synthetase. This led to the inhibition of free IAA combining with amino acid, resulting in excessive free IAA accumulation. Excessive free IAA alters plant tissue structure, accelerates fungal hyphal invasion, reduced the activity of antioxidant enzymes (SOD, POD and CAT) and increased reactive oxygen species (ROS) level, reduced total chlorophyll content and photosynthetic ability, while regulating the expression of PR-related genes including PR1, PR4, PR5 and PR8. It also changed the content of plant hormones and amino acids, and ultimately decreased the resistance to F. solani. In conclusion, these results demonstrate that MdGH3-2 and MdGH3-12 play an important role in F. solani tolerance to ARD.

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