4.7 Article

A Genome-Wide Analysis of the Pentatricopeptide Repeat Protein Gene Family in Two Kiwifruit Species with an Emphasis on the Role of RNA Editing in Pathogen Stress

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MDPI
DOI: 10.3390/ijms241813700

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pentatricopeptide repeat protein; pathogens infection; RNA editing; kiwifruit

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This study analyzed the PPR gene family in kiwifruit and found that PPRs play important roles in fruit development and disease resistance. Two PPR genes potentially involved in fruit development and maturation were identified, and differential expression of PPRs and RNA editing was observed between resistant and susceptible kiwifruits following infection with pathogenic bacteria.
Kiwifruit is a perennial fruit tree with high nutritional and economic value; however, various pathogen stresses have resulted in reductions in its yield and quality. Pentatricopeptide repeat proteins (PPRs), characterized by tandem repetitions of 35 amino acid motifs, play roles in RNA editing, mRNA stability, and splicing. They may also regulate plant development and growth. Nevertheless, the roles of PPRs in plant development and disease resistance remain unclear. In this study, we focused on the roles of PPRs in the fruit development and pathogen stress of kiwifruit and conducted a series of analyses of the PPR gene family in two representative kiwifruit species (Actinidia chinensis (Ach) and Actinidia eriantha (Ace)) with markedly different degrees of disease resistance. A total of 497 and 499 PPRs were identified in Ach and Ace, respectively. All the kiwifruit PPRs could be phylogenetically divided into four subfamilies. There were about 40.68% PPRs predicted to be localized to mitochondria or chloroplasts. A synteny analysis showed that the expansion of the kiwifruit PPRs mainly originated from segmental duplication. Based on RNA-seq data from the fruit over 12 periods of development and maturity, a weighted correlation network analysis suggested that two PPRs, Actinidia20495.t1 and Actinidia15159.t1, may be involved in fruit development and maturation. In addition, we observed different responses with respect to the expression of PPRs and RNA editing between resistant and susceptible kiwifruits following infection with pathogenic bacteria, indicating the regulatory role of PPRs in the stress response via the modulation of RNA editing. The differentially expressed upstream transcription factors of the PPRs were further identified; they may regulate resistance adaption by modulating the expression of the PPRs. Collectively, these results suggest that PPRs play roles in the development and disease resistance of kiwifruit and provide candidate genes for further clarifying the resistance mechanisms in kiwifruits.

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