Presentation Information
[P04-471]Identification of SLA1 as a Novel Gene Involved in Lipid Accumulation in the Oleaginous Yeast Lipomyces starkeyi
○Rikako Sato1, Harutake Yamazaki1, Yosuke Shida2, Wataru Ogasawara2, Hiroaki Takaku1 (1. Niigata University of Pharmacy and Medical and Life Sciences (Japan), 2. Nagaoka University of Technology (Japan))
Keywords:
Lipomyces starkeyi,Oleaginous yeast,TAG
Global population growth has increased demand for food and energy, while environmental degradation and climate change have become major challenges to achieving a sustainable society. To address these issues, production technologies that reduce dependence on fossil resources and efficiently utilize renewable resources are needed. Accordingly, microbial production of fuels and chemicals from renewable feedstocks such as biomass has attracted considerable attention. Oils produced by oleaginous microorganisms are attracting interest as sustainable alternatives to plant oils because of their similar fatty acid composition. The oleaginous yeast Lipomyces starkeyi is an attractive host for lipid production because it shows one of the highest lipid contents among oleaginous yeasts and can convert various carbon sources, including glucose, starch, glycerol, xylose, and cellobiose, into lipids. Despite these advantages, improving lipid productivity remains a key challenge for industrial application. To overcome this limitation, it is necessary to elucidate the mechanism underlying lipid production in L. starkeyi and apply this knowledge to improve productivity. In this study, we aimed to identify the gene responsible for the low-lipid-accumulation phenotype in sr22 by comparative genome analysis and to clarify how this gene affects lipid synthesis and degradation pathways.
Comparative genome analysis between the wild-type and sr22 identified SLA1 (suppressed lipid accumulation-related gene) as a candidate gene responsible for low lipid accumulation. Replacement of the wild-type SLA1 with the sr22-derived mutant SLA1L641P markedly reduced lipid productivity and reproduced the sr22 phenotype. In contrast, deletion of SLA1 increased lipid production compared with the wild-type. These results indicate that SLA1L641P is responsible for the low-lipid-accumulation phenotype of sr22 and that Sla1p functions as a negative regulator of lipid accumulation. Gene expression analysis of the SLA1L641P mutant and the SLA1 deletion strain showed that SLA1L641P not only downregulated genes involved in the acyl-CoA synthesis pathway, one of the TAG biosynthetic pathways, but also activated TAG degradation pathways, particularly β-oxidation, thereby contributing to low lipid productivity. In contrast, increased lipid production in the SLA1 deletion strain was likely associated with suppression of β-oxidation. These findings suggest that improving lipid productivity requires not only activation of lipid biosynthesis but also suppression of lipid degradation. Sla1p appears to negatively affect lipid accumulation by repressing acyl-CoA synthesis and promoting β-oxidation. This study identified Sla1p as a novel factor involved in lipid accumulation and provides a new target for improving TAG production in L. starkeyi.
This work was supported by the JSPS Program for Forming Japan’s Peak Research Universities (J-PEAKS) (Grant No. JPJS00420240017).
Comparative genome analysis between the wild-type and sr22 identified SLA1 (suppressed lipid accumulation-related gene) as a candidate gene responsible for low lipid accumulation. Replacement of the wild-type SLA1 with the sr22-derived mutant SLA1L641P markedly reduced lipid productivity and reproduced the sr22 phenotype. In contrast, deletion of SLA1 increased lipid production compared with the wild-type. These results indicate that SLA1L641P is responsible for the low-lipid-accumulation phenotype of sr22 and that Sla1p functions as a negative regulator of lipid accumulation. Gene expression analysis of the SLA1L641P mutant and the SLA1 deletion strain showed that SLA1L641P not only downregulated genes involved in the acyl-CoA synthesis pathway, one of the TAG biosynthetic pathways, but also activated TAG degradation pathways, particularly β-oxidation, thereby contributing to low lipid productivity. In contrast, increased lipid production in the SLA1 deletion strain was likely associated with suppression of β-oxidation. These findings suggest that improving lipid productivity requires not only activation of lipid biosynthesis but also suppression of lipid degradation. Sla1p appears to negatively affect lipid accumulation by repressing acyl-CoA synthesis and promoting β-oxidation. This study identified Sla1p as a novel factor involved in lipid accumulation and provides a new target for improving TAG production in L. starkeyi.
This work was supported by the JSPS Program for Forming Japan’s Peak Research Universities (J-PEAKS) (Grant No. JPJS00420240017).
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