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Research |
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Homeobox Transcription Factors Are Required for Fungal Development and the Suppression of Host Defense Mechanisms in the Colletotrichum scovillei-Pepper Pathosystem
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Authours
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Teng Fu, a Joon-Hee Han, b Jong-Hwan Shin, a Hyeunjeong Song, c Jaeho Ko, c Yong-Hwan Lee, c Ki-Tae Kim, d Kyoung Su Kima |
Title |
Homeobox Transcription Factors Are Required for Fungal Development and the Suppression of Host Defense Mechanisms in the Colletotrichum scovillei-Pepper Pathosystem |
Journal |
MBIO, 2021 (12) ~ |
Abstract
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Colletotrichum scovillei, an ascomycete phytopathogenic fungus, is the
main causal agent of serious yield losses of economic crops worldwide. The fungus
causes anthracnose disease on several fruits, including peppers. However, little is
known regarding the underlying molecular mechanisms involved in the development of anthracnose caused by this fungus. In an initial step toward understanding
the development of anthracnose on pepper fruits, we retrieved 624 transcription
factors (TFs) from the whole genome of C. scovillei and comparatively analyzed the
entire repertoire of TFs among phytopathogenic fungi. Evolution and proliferation
of members of the homeobox-like superfamily, including homeobox (HOX) TFs that
regulate the development of eukaryotic organisms, were demonstrated in the genus Colletotrichum. C. scovillei was found to contain 10 HOX TF genes (CsHOX1 to
CsHOX10), which were functionally characterized using deletion mutants of each
CsHOX gene. Notably, CsHOX1 was identified as a pathogenicity factor required for
the suppression of host defense mechanisms, which represents a new role for HOX
TFs in pathogenic fungi. CsHOX2 and CsHOX7 were found to play essential roles in
conidiation and appressorium development, respectively, in a stage-specific manner in C. scovillei. Our study provides a molecular basis for understanding the
mechanisms associated with the development of anthracnose on fruits caused by
C. scovillei, which will aid in the development of novel approaches for disease
management. |
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