Mid1 affects ion transport, cell wall integrity, and host penetration of the entomopathogenic fungus Metarhizium acridum

2019 ◽  
Vol 103 (4) ◽  
pp. 1801-1810 ◽  
Author(s):  
Mushan Xie ◽  
Xuan Zhou ◽  
Yuxian Xia ◽  
Yueqing Cao
2021 ◽  
Vol 7 (7) ◽  
pp. 512
Author(s):  
Chaochuang Li ◽  
Qipei Zhang ◽  
Yuxian Xia ◽  
Kai Jin

The nitrogen catabolite repression (NCR) pathway is involved in nitrogen utilization, in which the global GATA transcription factor AreA plays an indispensable role and has been reported in many fungi. However, relatively few studies are focused on AreB, another GATA transcription factor in the NCR pathway and the functions of AreB are largely unknown in entomopathogenic fungi. Here, we characterized MaAreB in the model entomopathogenic fungus Metarhizium acridum. Sequence arrangement found that MaAreB had a conserved GATA zinc finger DNA binding domain and a leucine zipper domain. Disruption of MaAreB affected the nitrogen utilization and led to decelerated conidial germination and hyphal growth, decreased conidial yield, and lower tolerances to UV-B irradiation and heat-shock. Furthermore, the MaAreB mutant (ΔMaAreB) exhibited increased sensitivity to CFW (Calcofluor white), decreased cell wall contents (chitin and β-1,3-glucan) and reduced expression levels of some genes related to cell wall integrity, indicating that disruption of MaAreB affected the cell wall integrity. Bioassays showed that the virulence of the ΔMaAreB strain was decreased in topical inoculation but not in intra-hemocoel injection. Consistently, deletion of MaAreB severely impaired the appressorium formation and reduced the turgor pressure of appressorium. These results revealed that MaAreB regulated fungal nitrogen utilization, cell wall integrity and biological control potential, which would contribute to the functional characterization of AreB homologous proteins in other insect fungal pathogens, and even filamentous fungi.


2019 ◽  
Vol 65 (4) ◽  
pp. 1025-1040 ◽  
Author(s):  
Tingting Zhao ◽  
Huiting Tian ◽  
Yuxian Xia ◽  
Kai Jin

2019 ◽  
Vol 15 (8) ◽  
pp. e1007964 ◽  
Author(s):  
Junjie Zhang ◽  
Hui Jiang ◽  
Yanru Du ◽  
Nemat O. Keyhani ◽  
Yuxian Xia ◽  
...  

2018 ◽  
Vol 16 (1) ◽  
pp. 44-53
Author(s):  
Marina Campos Rocha ◽  
Camilla Alves Santos ◽  
Iran Malavazi

Different signaling cascades including the Cell Wall Integrity (CWI), the High Osmolarity Glycerol (HOG) and the Ca2+/calcineurin pathways control the cell wall biosynthesis and remodeling in fungi. Pathogenic fungi, such as Aspergillus fumigatus and Candida albicans, greatly rely on these signaling circuits to cope with different sources of stress, including the cell wall stress evoked by antifungal drugs and the host’s response during infection. Hsp90 has been proposed as an important regulatory protein and an attractive target for antifungal therapy since it stabilizes major effector proteins that act in the CWI, HOG and Ca2+/calcineurin pathways. Data from the human pathogen C. albicans have provided solid evidence that loss-of-function of Hsp90 impairs the evolution of resistance to azoles and echinocandin drugs. In A. fumigatus, Hsp90 is also required for cell wall integrity maintenance, reinforcing a coordinated function of the CWI pathway and this essential molecular chaperone. In this review, we focus on the current information about how Hsp90 impacts the aforementioned signaling pathways and consequently the homeostasis and maintenance of the cell wall, highlighting this cellular event as a key mechanism underlying antifungal therapy based on Hsp90 inhibition.


2021 ◽  
Author(s):  
Ji-Zheng Song ◽  
Ya-Ping Yin ◽  
Wen Cheng ◽  
Jia-Hua Liu ◽  
Shun-Juan Hu ◽  
...  

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