纤维素反应转运体样蛋白 CRT2 在毛霉菌纤维素酶诱导过程中的作用

Su Yan, Yan Xu, Xiao-Wei Yu
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引用次数: 0

摘要

背景:纤维素溶解真菌毛霉中纤维素酶的诱导受到纤维素碳源的强烈激活。一般认为,纤维素诱导剂的转运和诱导信号的感知是纤维素酶诱导的关键过程,诱导信号将被雷氏毛霉中的糖转运体/受体感知。在诱导阶段,有多个糖转运体同时表达,但它们的功能是什么,如何协同工作,目前还很难阐明:在这项研究中,我们发现纤维素反应转运体样蛋白 CRT2(之前被鉴定为假定性乳糖渗透酶 TRE77517)的组成型表达能提高纤维素酶在纤维素、纤维生物糖或乳糖培养基上的诱导效果。功能研究表明,在酵母系统中,膜结合的 CRT2 不是纤维生物糖、乳糖或葡萄糖的转运体,它也不会影响雷氏菌对纤维生物糖和乳糖的利用。进一步研究发现,CRT2 在纤维素酶诱导方面的功能与纤维生物糖转运体 CRT1 略有相似。过表达 CRT2 会导致 CRT1 和关键转录因子 XYR1 的上调。此外,CRT2的过表达可部分弥补CRT1在纤维素酶诱导过程中的功能缺失:我们的研究发现了 CRT2 在纤维素酶诱导过程中与 CRT1 和 XYR1 协作的新功能,可能是一种信号传导因子。这些结果加深了人们对糖转运体在纤维素酶生产中的影响的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Role of cellulose response transporter-like protein CRT2 in cellulase induction in Trichoderma reesei.

Role of cellulose response transporter-like protein CRT2 in cellulase induction in Trichoderma reesei.

Role of cellulose response transporter-like protein CRT2 in cellulase induction in Trichoderma reesei.

Role of cellulose response transporter-like protein CRT2 in cellulase induction in Trichoderma reesei.

Background: Induction of cellulase in cellulolytic fungi Trichoderma reesei is strongly activated by cellulosic carbon sources. The transport of cellulosic inducer and the perception of inducing signal is generally considered as the critical process for cellulase induction, that the inducing signal would be perceived by a sugar transporter/transceptor in T. reesei. Several sugar transporters are coexpressed during the induction stage, but which function they serve and how they work collaboratively are still difficult to elucidate.

Results: In this study, we found that the constitutive expression of the cellulose response transporter-like protein CRT2 (previously identified as putative lactose permease TRE77517) improves cellulase induction on a cellulose, cellobiose or lactose medium. Functional studies indicate that the membrane-bound CRT2 is not a transporter of cellobiose, lactose or glucose in a yeast system, and it also does not affect cellobiose and lactose utilization in T. reesei. Further study reveals that CRT2 has a slightly similar function to the cellobiose transporter CRT1 in cellulase induction. Overexpression of CRT2 led to upregulation of CRT1 and the key transcription factor XYR1. Moreover, overexpression of CRT2 could partially compensate for the function loss of CRT1 on cellulase induction.

Conclusions: Our study uncovers the novel function of CRT2 in cellulase induction collaborated with CRT1 and XYR1, possibly as a signal transductor. These results deepen the understanding of the influence of sugar transporters in cellulase production.

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