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渗透胁迫反应、细胞壁完整性和分生孢子形成受一种组氨酸激酶传感器调控于…… (注:原文结尾处“in.”后面似乎缺少具体内容)

Osmotic Stress Responses, Cell Wall Integrity, and Conidiation Are Regulated by a Histidine Kinase Sensor in .

作者信息

Calcáneo-Hernández Gabriela, Landeros-Jaime Fidel, Cervantes-Chávez José Antonio, Mendoza-Mendoza Artemio, Esquivel-Naranjo Edgardo Ulises

机构信息

Unit for Basic and Applied Microbiology, Faculty of Natural Sciences, Autonomous University of Queretaro, Queretaro 76230, Mexico.

Departamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad de México 04510, Mexico.

出版信息

J Fungi (Basel). 2023 Sep 16;9(9):939. doi: 10.3390/jof9090939.

DOI:10.3390/jof9090939
PMID:37755046
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10532544/
Abstract

responds to various environmental stressors through the mitogen-activated protein kinase (MAPK) Tmk3 and MAPK-kinase Pbs2 signaling pathways. In fungi, orthologues to Tmk3 are regulated by a histidine kinase (HK) sensor. However, the role of HKs remains unknown. In this regard, the function of the HK Nik1 was analyzed in response to stressors regulated by Tmk3. The growth of the Δ mutant strains was compromised under hyperosmotic stress; mycelia were less resistant to lysing enzymes than the WT strain, while conidia of Δ were more sensitive to Congo red; however, ∆ and ∆ strains showed a more drastic defect in cell wall stability. Light-regulated and gene expression was induced upon an osmotic shock through Pbs2-Tmk3 but was independent of Nik1. The encoding chitin synthases and genes were downregulated after an osmotic shock in the WT, but and expression were enhanced in ∆, ∆, and ∆. The vegetative growth and conidiation by light decreased in ∆, although Nik1 was unrequired to activate the light-responsive genes by Tmk3. Altogether, Nik1 regulates responses related to the Pbs2-Tmk3 pathway and suggests the participation of additional HKs to respond to stress.

摘要

通过丝裂原活化蛋白激酶(MAPK)Tmk3和MAPK激酶Pbs2信号通路对各种环境应激源作出反应。在真菌中,Tmk3的直系同源物受组氨酸激酶(HK)传感器调节。然而,HKs的作用仍然未知。在这方面,分析了HK Nik1在响应由Tmk3调节的应激源时的功能。Δ突变菌株的生长在高渗胁迫下受到损害;菌丝体对裂解酶的抗性低于野生型菌株,而Δ的分生孢子对刚果红更敏感;然而,Δ和Δ菌株在细胞壁稳定性方面表现出更严重的缺陷。通过Pbs2-Tmk3在渗透休克后诱导光调节的和基因表达,但与Nik1无关。在野生型中,编码几丁质合酶和的基因在渗透休克后下调,但在Δ、Δ和Δ中,和的表达增强。尽管激活Tmk3的光响应基因不需要Nik1,但Δ中的营养生长和光诱导的分生孢子形成减少。总之,Nik1调节与Pbs2-Tmk3途径相关的反应,并表明其他HKs参与应激反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/83f24c44e3b2/jof-09-00939-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/00db10946e57/jof-09-00939-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/808b8b250261/jof-09-00939-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/a9526bfc2692/jof-09-00939-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/c9945f556578/jof-09-00939-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/1273a8a51a1a/jof-09-00939-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/83f24c44e3b2/jof-09-00939-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/00db10946e57/jof-09-00939-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/808b8b250261/jof-09-00939-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/a9526bfc2692/jof-09-00939-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/c9945f556578/jof-09-00939-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/1273a8a51a1a/jof-09-00939-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9071/10532544/83f24c44e3b2/jof-09-00939-g006.jpg

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