AoSsk1, a Response Regulator Required for Mycelial Growth and Development, Stress Responses, Trap Formation, and the Secondary Metabolism in Arthrobotrys oligospora .
Ke-Xin JiangQian-Qian LiuNa BaiMei-Chen ZhuKe-Qin ZhangJin-Kui YangPublished in: Journal of fungi (Basel, Switzerland) (2022)
Ssk1, a response regulator of the two-component signaling system, plays an important role in the cellular response to hyperosmotic stress in fungi. Herein, an ortholog of ssk1 ( Ao ssk1 ) was characterized in the nematode-trapping fungus Arthrobotrys oligospora using gene disruption and multi-phenotypic comparison. The deletion of Aossk1 resulted in defective growth, deformed and swollen hyphal cells, an increased hyphal septum, and a shrunken nucleus. Compared to the wild-type (WT) strain, the number of autophagosomes and lipid droplets in the hyphal cells of the Δ Aossk1 mutant decreased, whereas their volumes considerably increased. Aossk1 disruption caused a 95% reduction in conidial yield and remarkable defects in tolerance to osmotic and oxidative stress. Meanwhile, the transcript levels of several sporulation-related genes were significantly decreased in the Δ Aossk1 mutant compared to the WT strain, including abaA , brlA , flbC , fluG , and rodA . Moreover, the loss of Aossk1 resulted in a remarkable increase in trap formation and predation efficiency. In addition, many metabolites were markedly downregulated in the Δ Aossk1 mutant compared to the WT strain. Our results highlight that AoSsk1 is a crucial regulator of asexual development, stress responses, the secondary metabolism, and pathogenicity, and can be useful in probing the regulatory mechanism underlying the trap formation and lifestyle switching of nematode-trapping fungi.
Keyphrases
- wild type
- induced apoptosis
- candida albicans
- oxidative stress
- transcription factor
- cell cycle arrest
- endoplasmic reticulum stress
- biofilm formation
- cardiovascular disease
- metabolic syndrome
- ms ms
- signaling pathway
- genome wide
- cell death
- copy number
- ischemia reperfusion injury
- weight loss
- stress induced
- dna methylation
- cystic fibrosis
- escherichia coli
- pseudomonas aeruginosa
- heat stress
- genome wide analysis