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The transmembrane protein MaSho1 negatively regulates conidial yield by shifting the conidiation pattern in Metarhizium acridum
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 Metar...
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Published in: | Applied microbiology and biotechnology 2020-05, Vol.104 (9), p.4005-4015 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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
. |
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ISSN: | 0175-7598 1432-0614 |
DOI: | 10.1007/s00253-020-10523-0 |