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Published on: February 8, 2019
The transmembrane protein MaSho1 negatively regulates conidial yield by shifting the conidiation pattern in
Tingting Zhao1,2,3, Zhiqiong Wen1,2,3, Yuxian Xia4,5,6
1Genetic Engineering Research Center, School of Life Sciences, Chongqing University, Chongqing, 401331, People's Republic of China.
Abstract:
Sho1 is an important membrane sensor upstream of the HOG-MAPK signaling pathway, which plays critical roles in osmotic pressure response, growth, and virulence in fungi. Here, a Sho1 homolog (MaSho1), containing four transmembrane domains and one Src homology (SH3) domain, was characterized in Metarhizium acridum, a fungal pathogen of locusts. Targeted gene disruption of MaSho1 impaired cell wall integrity, virulence, and tolerances to UV-B and oxidative stresses, while none of them was affected when the SH3 domain was deleted. Intriguingly, disruption of MaSho1 significantly increased conidial yield, which was not affected in the SH3 domain mutant. Furthermore, it was found that deletion of MaSho1 led to microcycle conidiation of M. acridum on the normal conidiation medium. Deletion of MaSho1 significantly shortened the hyphal cells but had no effect on conidial germination. Digital gene expression profiling during conidiation indicated that differential expression of genes was associated with mycelial development, cell division, and differentiation between the wild type and the MaSho1 mutant. These data suggested that disruption of MaSho1 shifted the conidiation pattern by altering the transcription of genes to inhibit mycelial growth, thereby promoting the conidiation of M. acridum.
Insights
Disrupting the Sho1 homolog (MaSho1) in Metarhizium acridum altered fungal development. MaSho1 deletion promoted conidial yield and microcycle conidiation by affecting gene expression.
Area of Science:
- Mycology
- Molecular Biology
- Signaling Pathways
Background:
- Sho1 acts as a membrane sensor in the HOG-MAPK pathway, crucial for fungal osmotic stress response, growth, and virulence.
- Metarhizium acridum is a significant fungal pathogen affecting locusts.
Purpose of the Study:
- To characterize the function of a Sho1 homolog (MaSho1) in Metarhizium acridum.
- To investigate the role of MaSho1 in fungal development, stress tolerance, and virulence.
Main Methods:
- Targeted gene disruption of MaSho1 and its SH3 domain.
- Phenotypic analysis of mutants, including cell wall integrity, stress tolerance, and conidiation.
- Digital gene expression profiling during conidiation.
Main Results:
- MaSho1 disruption impaired cell wall integrity, virulence, and UV-B/oxidative stress tolerance, but not conidial germination.
- MaSho1 deletion significantly increased conidial yield and induced microcycle conidiation.
- Differential gene expression in MaSho1 mutants revealed altered pathways related to mycelial development and differentiation.
Conclusions:
- MaSho1 is essential for maintaining fungal cell wall integrity, virulence, and stress resistance in M. acridum.
- MaSho1 negatively regulates conidiation, and its disruption promotes conidial yield and microcycle conidiation by altering gene transcription.
- The SH3 domain of MaSho1 is not essential for its roles in virulence, stress tolerance, or conidiation pattern.
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