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<p>Autophagy is a cellular recycling process degrading and reusing cytoplasmic components via lysosomes or vacuoles, whereas lipophagy is a specialized form of autophagy that degrades lipid droplets (LDs). Thraustochytrids are heterotrophic marine protists known for high polyunsaturated fatty acid (PUFA) production and as valuable models for lipid metabolism research. In this study, LD degradation in <i>Aurantiochytrium limacinum</i> mh0186 was characterized under glucose-starvation conditions. Glucose starvation robustly activated autophagy, evidenced by GFP-tagged autophagy-related protein 8 (Atg8) translocation into endosome-like vesicles. These vesicles engulfed LDs in a microautophagy-like process, later fusing with acidic vacuole-like organelles (VLOs) to facilitate LD degradation. Impaired autophagy inhibited LD degradation in endosome-like vesicles but triggered compensatory lipolysis through elevation of intracellular lipase activity, resulting in a significant decrease in triacylglycerol (TG) levels. Our findings revealed a dual regulatory network in which autophagy orchestrated LD degradation via endosome-like vesicles, whereas autophagy inhibition triggered compensatory lipolysis activation to sustain lipid degradation.</p>

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Lipid Droplet Degradation Through Lipophagy in Aurantiochytrium limacinum mh0186

  • 期刊论文

  • 发表日期：

    2025年8月2日

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  • Sheng Wu,
  • Yohei Ishibashi,
  • Masahiro Hayashi,
  • Nozomu Okino

摘要

Autophagy is a cellular recycling process degrading and reusing cytoplasmic components via lysosomes or vacuoles, whereas lipophagy is a specialized form of autophagy that degrades lipid droplets (LDs). Thraustochytrids are heterotrophic marine protists known for high polyunsaturated fatty acid (PUFA) production and as valuable models for lipid metabolism research. In this study, LD degradation in Aurantiochytrium limacinum mh0186 was characterized under glucose-starvation conditions. Glucose starvation robustly activated autophagy, evidenced by GFP-tagged autophagy-related protein 8 (Atg8) translocation into endosome-like vesicles. These vesicles engulfed LDs in a microautophagy-like process, later fusing with acidic vacuole-like organelles (VLOs) to facilitate LD degradation. Impaired autophagy inhibited LD degradation in endosome-like vesicles but triggered compensatory lipolysis through elevation of intracellular lipase activity, resulting in a significant decrease in triacylglycerol (TG) levels. Our findings revealed a dual regulatory network in which autophagy orchestrated LD degradation via endosome-like vesicles, whereas autophagy inhibition triggered compensatory lipolysis activation to sustain lipid degradation.