Molecular insights into the response of Acidithiobacillus caldus to leached metal toxicity during bioleaching of spent FCC catalyst

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Abstract Acidithiobacillus caldus , a thermoacidophilic sulfur-oxidizing bacterium, is utilized in bioleaching owing to its robust metabolic capabilities.To elucidate the adaptive mechanisms of A. caldus to metal toxicity during bioleaching of spent fluid catalytic cracking catalyst (SFCCC), an integrated approach was employed, encompassing dynamic monitoring of metal release, enzymatic activity assays, and de novo transcriptome sequencing. This study systematically deciphered the synergistic mechanism of “leaching promotion–toxicity response–resistance regulation” in A. caldus under SFCCC-induced stress. The bacterium demonstrated high leaching efficiency of heavy metals from SFCCC. Under metal-induced stress, it employed defense mechanisms primarily through a glutathione peroxidase (GSH-Px)-mediated antioxidant system. This response was sustained by the continuous activation of H⁺-ATPase and NADPH-generating metabolic pathways to maintain energy and reduce supply. The bacterial response exhibited concentration dependence: under low-concentration stress, it prioritized basal metabolic maintenance alongside initiation of defensive measures; under high-concentration stress, it employed a comprehensive survival strategy involving metabolic reprogramming to sacrifice non-essential functions in favor of critical survival processes. This transition reflects a strategic shift from a “growth-oriented” to a “survival-oriented” mode. These findings enhance the theoretical framework for understanding concentration-dependent strategic transitions in microbe-metal interactions and offer a molecular biology basis for improving the practical application of bioleaching technologies.
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Molecular insights into the response of Acidithiobacillus caldus to leached metal toxicity during bioleaching of spent FCC catalyst | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Molecular insights into the response of Acidithiobacillus caldus to leached metal toxicity during bioleaching of spent FCC catalyst Lu Zheng, Yue-jie Wang, Ling-ling Li, Sheng Zhao, Chang-yun Zhang, and 1 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7655028/v1 This work is licensed under a CC BY 4.0 License Status: Under Revision Version 1 posted 9 You are reading this latest preprint version Abstract Acidithiobacillus caldus , a thermoacidophilic sulfur-oxidizing bacterium, is utilized in bioleaching owing to its robust metabolic capabilities.To elucidate the adaptive mechanisms of A. caldus to metal toxicity during bioleaching of spent fluid catalytic cracking catalyst (SFCCC), an integrated approach was employed, encompassing dynamic monitoring of metal release, enzymatic activity assays, and de novo transcriptome sequencing. This study systematically deciphered the synergistic mechanism of “leaching promotion–toxicity response–resistance regulation” in A. caldus under SFCCC-induced stress. The bacterium demonstrated high leaching efficiency of heavy metals from SFCCC. Under metal-induced stress, it employed defense mechanisms primarily through a glutathione peroxidase (GSH-Px)-mediated antioxidant system. This response was sustained by the continuous activation of H⁺-ATPase and NADPH-generating metabolic pathways to maintain energy and reduce supply. The bacterial response exhibited concentration dependence: under low-concentration stress, it prioritized basal metabolic maintenance alongside initiation of defensive measures; under high-concentration stress, it employed a comprehensive survival strategy involving metabolic reprogramming to sacrifice non-essential functions in favor of critical survival processes. This transition reflects a strategic shift from a “growth-oriented” to a “survival-oriented” mode. These findings enhance the theoretical framework for understanding concentration-dependent strategic transitions in microbe-metal interactions and offer a molecular biology basis for improving the practical application of bioleaching technologies. Acidithiobacillus caldus spent FCC catalyst heavy metal toxicity response mechanisms Full Text Additional Declarations No competing interests reported. Supplementary Files S1.xlsx Cite Share Download PDF Status: Under Revision Version 1 posted Editorial decision: Revision requested 19 May, 2026 Reviews received at journal 18 May, 2026 Reviews received at journal 06 May, 2026 Reviewers agreed at journal 29 Apr, 2026 Reviewers agreed at journal 26 Apr, 2026 Reviewers invited by journal 05 Nov, 2025 Editor assigned by journal 24 Sep, 2025 Submission checks completed at journal 24 Sep, 2025 First submitted to journal 19 Sep, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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