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铜转运蛋白 CrpF 可防止. 中铜诱导的毒性。

Cu transporter protein CrpF protects against Cu-induced toxicity in .

机构信息

Unitat de Microbiologia, Facultat de Medicina i Ciències de la Salut and Institut d'Investigació Sanitària Pere Virgili (IISPV), Universitat Rovira i Virgili , Reus, Spain.

Departamento de Genetica, Facultad de Ciencias and Campus De Excelencia Internacional Agroalimentario ceiA3, Universidad de Cordoba , Cordoba, Spain.

出版信息

Virulence. 2020 Dec;11(1):1108-1121. doi: 10.1080/21505594.2020.1809324.

DOI:10.1080/21505594.2020.1809324
PMID:32862758
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7549990/
Abstract

Cu is an essential trace element for cell growth and proliferation. However, excess of Cu accumulation leads to cellular toxicity. Thus, precise and tight regulation of Cu homeostasis processes, including transport, delivery, storage, detoxification, and efflux machineries, is required. Moreover, the maintenance of Cu homeostasis is critical for the survival and virulence of fungal pathogens. Cu homeostasis has been extensively studied in mammals, bacteria, and yeast, but it has not yet been well documented in filamentous fungi. In the present work, we investigated Cu tolerance in the filamentous fungus by analysing the Cu transporter coding gene , previously studied in . The expression studies demonstrated that is upregulated in the presence of Cu and its deletion leads to severe sensitivity to low levels of CuSO in . Targeted deletion of did not significantly alter the resistance of the fungus to macrophage killing, nor its pathogenic behaviour on the tomato plants. However, the targeted deletion mutant Δ showed increased virulence in a murine model of systemic infection compared to wild-type strain (wt).

摘要

铜是细胞生长和增殖所必需的微量元素。然而,过量的铜积累会导致细胞毒性。因此,需要精确和严格地调节铜的动态平衡过程,包括运输、传递、储存、解毒和外排机制。此外,维持铜的动态平衡对真菌病原体的生存和毒力至关重要。铜的动态平衡在哺乳动物、细菌和酵母中得到了广泛研究,但在丝状真菌中尚未得到很好的记录。在本工作中,我们通过分析先前在 中研究过的铜转运蛋白编码基因 ,研究了丝状真菌 的铜耐受性。表达研究表明, 在铜存在的情况下上调,其缺失导致对低水平的 CuSO 在 中非常敏感。 的靶向缺失并未显著改变真菌对巨噬细胞杀伤的抗性,也未改变其在番茄植株上的致病性行为。然而,与野生型菌株 (wt) 相比,靶向缺失突变体 Δ 在系统性感染的小鼠模型中表现出更高的毒力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/dab89e5e7566/KVIR_A_1809324_F0007_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/ea3c5fabaa9f/KVIR_A_1809324_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/12f332b16569/KVIR_A_1809324_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/7c79e4e8f18f/KVIR_A_1809324_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/1ca785ffd723/KVIR_A_1809324_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/6d449bd9b3cf/KVIR_A_1809324_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/caa36a258017/KVIR_A_1809324_F0006_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/dab89e5e7566/KVIR_A_1809324_F0007_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/ea3c5fabaa9f/KVIR_A_1809324_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/12f332b16569/KVIR_A_1809324_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/7c79e4e8f18f/KVIR_A_1809324_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/1ca785ffd723/KVIR_A_1809324_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/6d449bd9b3cf/KVIR_A_1809324_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/caa36a258017/KVIR_A_1809324_F0006_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adb2/7549990/dab89e5e7566/KVIR_A_1809324_F0007_B.jpg

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