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糖原储存中的遗传调节因子及其生理意义

Genetic Regulators and Physiological Significance of Glycogen Storage in .

作者信息

Zeitz Marcus A, Tanveer Zainab, Openshaw Anatole T, Schmidt Martin

机构信息

Department of Biochemistry and Nutrition, College of Osteopathic Medicine, Des Moines University, 3200 Grand Avenue, Des Moines, IA 50312, USA.

出版信息

J Fungi (Basel). 2019 Oct 30;5(4):102. doi: 10.3390/jof5040102.

Abstract

The dimorphic human fungal pathogen has broad metabolic flexibility that allows it to adapt to the nutrient conditions in different host habitats. builds large carbohydrate stores (glycogen) at the end of exponential growth and begins consumption of stored carbohydrates when nutrients become limiting. The expression of genes required for the successful transition between host environments, including the factors controlling glycogen content, is controlled by protein kinase A signaling through the transcription factor Efg1. In addition to the inability to transition to hyphal growth, mutants have low glycogen content and reduced long-term survival, suggesting that carbohydrate storage is required for viability during prolonged culture. To test this assumption, we constructed a glycogen-deficient mutant and assessed its viability during extended culture. Pathways and additional genetic factors controlling glycogen synthesis were identified through the screening of mutant libraries for strains with low glycogen content. Finally, a part of the Efg1-regulon was screened for mutants with a shortened long-term survival phenotype. We found that glycogen deficiency does not affect long-term survival, growth, metabolic flexibility or morphology of . We conclude that glycogen is not an important contributor to fitness.

摘要

这种双态性人类真菌病原体具有广泛的代谢灵活性,使其能够适应不同宿主栖息地的营养条件。在指数生长末期积累大量碳水化合物储备(糖原),当营养物质变得有限时开始消耗储存的碳水化合物。在宿主环境之间成功转变所需的基因表达,包括控制糖原含量的因子,由蛋白激酶A通过转录因子Efg1进行信号传导来调控。除了无法转变为菌丝生长外,突变体的糖原含量低且长期存活率降低,这表明在长期培养过程中碳水化合物储存对于生存能力是必需的。为了验证这一假设,我们构建了一个糖原缺陷型突变体,并评估其在延长培养期间的生存能力。通过筛选糖原含量低的菌株的突变体文库,确定了控制糖原合成的途径和其他遗传因素。最后,对Efg1调控子的一部分进行筛选,寻找具有缩短的长期存活表型的突变体。我们发现糖原缺乏并不影响该病原体的长期存活、生长、代谢灵活性或形态。我们得出结论,糖原对该病原体的适应性并非重要贡献因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8567/6958490/e55916d595b5/jof-05-00102-g001.jpg

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