Transcription Factor VM1G_06867: A Requirement for Growth, Pathogenicity, Development, and Maintenance of Cell Wall Integrity in Valsa mali

Author:

Diao Yufei1,Jin Jiyang2ORCID,Xiong Xiong2,Yu Chengming1,Tian Yehan1,Li Duochuan1,Liu Huixiang1

Affiliation:

1. Shandong Research Center for Forestry Harmful Biological Control Engineering and Technology, College of Plant Protection, Shandong Agricultural University, Tai’an 271018, China

2. Mountain Tai Forest Ecosystem Research Station of State Forestry Administration, Forestry College, Shandong Agricultural University, Tai’an 271018, China

Abstract

Apple canker disease, caused by Valsa mali, is one of the most serious apple tree diseases in China. VmSom1 is an important transcription factor that acts on the cyclic adenosine signaling pathway (cAMP/PKA), regulating the growth, development, morphological differentiation, and pathogenic forces of the pathogen. We perform transcriptome analysis of the VmSom1 deletion mutant and the wild-type strain 11-175 and identify a significantly differentially expressed gene, VM1G_06867, a zinc finger motif transcription factor in V. mali. In this study, we obtain the VM1G_06867 gene using the single deletion mutant via homologous recombination. To determine the relationship between VmSom1 and VM1G_06867, we also obtain a double deletion mutant ΔVmSom1/06867. Compared to the wild-type strain 11-175, the single deletion mutant VM1G_06867 shows a drastic reduction in growth rate and forms more pycnidia on the PDA medium. Additionally, the growth of the mutant is inhibited by SDS, Congo red, and fluorescent brighteners. In comparison to the single deletion mutant VmSom1, the double deletion mutant ΔVmSom1/06867 shows no significant change in growth or conidiation and is unable to produce conidia. The growth rate is significantly increased in Congo red, NaCl, and Sorbitol mediums. These results demonstrate that VM1G_06867 plays important roles in growth, pathogenicity, asexual development, and maintenance of cell wall integrity. VM1G_06867 can recover osmotic stress and cell wall integrity defects caused by the deletion of VmSom1, as well as restore the loss of pathogenicity caused by the deletion of the VmSom1 gene, but not completely.

Funder

National Natural Science Foundation of China

Innovation Project of Forestry Science and Technology

Publisher

MDPI AG

Subject

Plant Science,Ecology, Evolution, Behavior and Systematics,Microbiology (medical)

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