Scholarlink

Abstract <p>β-Glucosidases (EC 3.2.1.21) are essential enzymes involved in biomass degradation and metabolic regulation, but the physiological roles of intracellular β-glucosidases in filamentous fungi remain incompletely understood. In this study, we characterized CbgA (AN10124) and CbgB (AN10375), two intracellular glycoside hydrolase family 1 β-glucosidases, in <i>Aspergillus nidulans</i>. Gene deletion and biochemical analyses demonstrated that CbgA is the predominant intracellular β-glucosidase. Loss of <i>cbgA</i> led to overactivation of cellulases, cellobiose-dependent accumulation of reddish-brown secondary metabolites, and a significant reduction in conidiation. Crucially, deletion of the cellobiose transporter gene <i>cltB</i> in the Δ<i>cbgA</i> background markedly attenuated these phenotypes, providing direct genetic evidence that the Δ<i>cbgA</i>-associated defects are driven by intracellular cellobiose accumulation rather than energy deficiency. Our findings identify CbgA as a critical “signal gatekeeper” that modulates the intensity of cellobiose-dependent induction. By maintaining the intracellular cellobiose pool within a physiological range, CbgA prevents secretory overload and maintains the metabolic balance between primary development and secondary metabolism. This study clarifies the coordination between nutrient transport and intracellular metabolism in shaping global regulatory outputs, suggesting that the targeted modulation of CbgA activity represents a potential strategy for optimizing cellulase production in fungal cell factories.</p> Key points <p><UnorderedList Mark="Bullet"> <ItemContent> <p><i>CbgA negatively regulates cellulase expression by controlling intracellular cellobiose levels.</i></p> </ItemContent> <ItemContent> <p><i>Loss of cbgA leads to hyperpigmentation and reduced conidiation on cellobiose.</i></p> </ItemContent> <ItemContent> <p><i>Deletion of cltB alleviates ΔcbgA phenotypes, confirming the role of intracellular cellobiose.</i></p> </ItemContent> </UnorderedList></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Intracellular β-glucosidase regulates cellulase expression and development in Aspergillus nidulans

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月4日

查看全文
  • Shun Yakabe,
  • Chihiro Kadooka,
  • Tomohiko Matsuzawa,
  • Yuzuki Kawai,
  • Masayuki Noguchi,
  • Daisuke Hira,
  • Masatoshi Goto,
  • Takuji Oka

摘要

Abstract

β-Glucosidases (EC 3.2.1.21) are essential enzymes involved in biomass degradation and metabolic regulation, but the physiological roles of intracellular β-glucosidases in filamentous fungi remain incompletely understood. In this study, we characterized CbgA (AN10124) and CbgB (AN10375), two intracellular glycoside hydrolase family 1 β-glucosidases, in Aspergillus nidulans. Gene deletion and biochemical analyses demonstrated that CbgA is the predominant intracellular β-glucosidase. Loss of cbgA led to overactivation of cellulases, cellobiose-dependent accumulation of reddish-brown secondary metabolites, and a significant reduction in conidiation. Crucially, deletion of the cellobiose transporter gene cltB in the ΔcbgA background markedly attenuated these phenotypes, providing direct genetic evidence that the ΔcbgA-associated defects are driven by intracellular cellobiose accumulation rather than energy deficiency. Our findings identify CbgA as a critical “signal gatekeeper” that modulates the intensity of cellobiose-dependent induction. By maintaining the intracellular cellobiose pool within a physiological range, CbgA prevents secretory overload and maintains the metabolic balance between primary development and secondary metabolism. This study clarifies the coordination between nutrient transport and intracellular metabolism in shaping global regulatory outputs, suggesting that the targeted modulation of CbgA activity represents a potential strategy for optimizing cellulase production in fungal cell factories.

Key points

CbgA negatively regulates cellulase expression by controlling intracellular cellobiose levels.

Loss of cbgA leads to hyperpigmentation and reduced conidiation on cellobiose.

Deletion of cltB alleviates ΔcbgA phenotypes, confirming the role of intracellular cellobiose.