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内切几丁质酶MaCts1参与分生孢子萌发、分生孢子产量、胁迫耐受性及短循环分生孢子形成过程 。 (你提供的原文最后有个不完整的点,这里按照正常补充完整意思翻译了)

MaCts1, an Endochitinase, Is Involved in Conidial Germination, Conidial Yield, Stress Tolerances and Microcycle Conidiation in .

作者信息

Zou Yuneng, Li Chan, Wang Shuqin, Xia Yuxian, Jin Kai

机构信息

Genetic Engineering Research Center, School of Life Sciences, Chongqing University, Chongqing 401331, China.

Chongqing Engineering Research Center for Fungal Insecticide, Chongqing 401331, China.

出版信息

Biology (Basel). 2022 Nov 29;11(12):1730. doi: 10.3390/biology11121730.

Abstract

Entomopathogenic fungi are promising biocontrol agents of insect-mediated crop damage. Microcycle conidiation has shown great potential in enhancing the conidial yield and quality of entomopathogenic fungi. Homologs of Cts1, an endochitinase of , participate in cell separation in several fungal spp. and may contribute to the morphological differences that occur during the shift to microcycle conidiation. However, the precise functions of in entomopathogenic fungi remain unclear. Herein, the endochitinase gene, , was characterized in the model entomopathogen, . A loss of function line for led to a delay of 1 h in the median germination time, a 28% reduction in conidial yield and significant defects in fungal resistances to UV-irradiation (18%) and heat-shock (15%), while fungal tolerances to cell wall stressors, oxidative and hyperosmotic stresses and virulence remained unchanged. The -disruption strain displayed typical conidiation on the microcycle conidiation induction medium, SYA. In contrast, deletion of key genes in the morphogenesis-related NDR kinase network (MOR pathway)/regulation of Ace2 and morphogenesis (RAM pathway) did not affect the SYA-induction of microcycle conidiation. This indicates that makes contributions to the microcycle conidiation, which may not be dependent on the MOR/RAM pathway in .

摘要

昆虫病原真菌是控制昆虫介导的作物损害的有前景的生物防治剂。微循环产孢在提高昆虫病原真菌的分生孢子产量和质量方面显示出巨大潜力。几丁质内切酶Cts1的同源物参与了几种真菌的细胞分离,并且可能导致向微循环产孢转变过程中出现的形态差异。然而,其在昆虫病原真菌中的具体功能仍不清楚。在此,对模式昆虫病原菌中的几丁质内切酶基因进行了表征。该基因功能缺失株的分生孢子萌发中值时间延迟1小时,分生孢子产量降低28%,并且对紫外线照射(18%)和热休克(15%)的真菌抗性存在显著缺陷,而对细胞壁应激源、氧化应激和高渗应激的耐受性以及毒力保持不变。该基因破坏菌株在微循环产孢诱导培养基SYA上表现出典型的产孢。相比之下,形态发生相关的NDR激酶网络(MOR途径)/Ace2调控和形态发生(RAM途径)中的关键基因缺失并不影响SYA诱导的微循环产孢。这表明该基因对微循环产孢有贡献,这可能不依赖于该病原菌中的MOR/RAM途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e58/9774441/2a866c469f25/biology-11-01730-g001.jpg

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