The apicoplast localized isocitrate dehydrogenase is needed for de novo fatty acid synthesis in the apicoplast of Toxoplasma gondii

Toxoplasma gondii (T. gondii), an apicomplexan parasite, infects a wide range of warm-blooded animals and poses significant risks to human health. The fatty acid synthesis II (FASII) pathway in the apicoplast, which is the major source of fatty acids in parasites, is considered a potential drug targ...

Full description

Saved in:
Bibliographic Details
Main Authors: Ke Pan, Ao Zeng, Xiaodie Ruan, Xinyu Mo, Bang Shen, Junlong Zhao, Yanqin Zhou
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-06-01
Series:Frontiers in Cellular and Infection Microbiology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcimb.2025.1542122/full
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850166054870843392
author Ke Pan
Ao Zeng
Xiaodie Ruan
Xinyu Mo
Bang Shen
Junlong Zhao
Yanqin Zhou
author_facet Ke Pan
Ao Zeng
Xiaodie Ruan
Xinyu Mo
Bang Shen
Junlong Zhao
Yanqin Zhou
author_sort Ke Pan
collection DOAJ
description Toxoplasma gondii (T. gondii), an apicomplexan parasite, infects a wide range of warm-blooded animals and poses significant risks to human health. The fatty acid synthesis II (FASII) pathway in the apicoplast, which is the major source of fatty acids in parasites, is considered a potential drug target. The apicoplast also harbors some enzymes of central carbon metabolism, which are crucial for its survival, but their biological roles remain unclear. In this study, we focused on apicoplast-localized isocitrate dehydrogenase 1 (ICDH1) and deleted it using CRISPR-Cas9 technology. The Δicdh1 mutant tachyzoites displayed markedly impaired growth kinetics, with further suppression under serum-deprived conditions. However, this deletion did not affect the viability or virulence of the Δicdh1 mutant in mice. NADPH, a product of ICDH1-mediated decarboxylation of isocitrate, is an essential cofactor for fatty acid synthesis. Using ¹³C6 glucose as a metabolic carbon source, we showed that the mutant strains had reduced incorporation of glucose-derived carbons into medium-chain length fatty acids (C14:0 and C16:0). Additionally, the growth of the mutant was partially restored by supplementation with exogenous C14:0 and C16:0 fatty acids. These results indicate that ICDH1 deletion affects the FASII pathway and parasite growth. Consistent with previous studies, this study confirms that T. gondii has metabolic flexibility in the apicoplast that allows it to acquire fatty acids through various pathways.
format Article
id doaj-art-bec33bc0cadf450a9957d2672fe5d076
institution OA Journals
issn 2235-2988
language English
publishDate 2025-06-01
publisher Frontiers Media S.A.
record_format Article
series Frontiers in Cellular and Infection Microbiology
spelling doaj-art-bec33bc0cadf450a9957d2672fe5d0762025-08-20T02:21:34ZengFrontiers Media S.A.Frontiers in Cellular and Infection Microbiology2235-29882025-06-011510.3389/fcimb.2025.15421221542122The apicoplast localized isocitrate dehydrogenase is needed for de novo fatty acid synthesis in the apicoplast of Toxoplasma gondiiKe PanAo ZengXiaodie RuanXinyu MoBang ShenJunlong ZhaoYanqin ZhouToxoplasma gondii (T. gondii), an apicomplexan parasite, infects a wide range of warm-blooded animals and poses significant risks to human health. The fatty acid synthesis II (FASII) pathway in the apicoplast, which is the major source of fatty acids in parasites, is considered a potential drug target. The apicoplast also harbors some enzymes of central carbon metabolism, which are crucial for its survival, but their biological roles remain unclear. In this study, we focused on apicoplast-localized isocitrate dehydrogenase 1 (ICDH1) and deleted it using CRISPR-Cas9 technology. The Δicdh1 mutant tachyzoites displayed markedly impaired growth kinetics, with further suppression under serum-deprived conditions. However, this deletion did not affect the viability or virulence of the Δicdh1 mutant in mice. NADPH, a product of ICDH1-mediated decarboxylation of isocitrate, is an essential cofactor for fatty acid synthesis. Using ¹³C6 glucose as a metabolic carbon source, we showed that the mutant strains had reduced incorporation of glucose-derived carbons into medium-chain length fatty acids (C14:0 and C16:0). Additionally, the growth of the mutant was partially restored by supplementation with exogenous C14:0 and C16:0 fatty acids. These results indicate that ICDH1 deletion affects the FASII pathway and parasite growth. Consistent with previous studies, this study confirms that T. gondii has metabolic flexibility in the apicoplast that allows it to acquire fatty acids through various pathways.https://www.frontiersin.org/articles/10.3389/fcimb.2025.1542122/fullToxoplasma gondiiapicoplastisocitrate dehydrogensasemetabolismFAS 2
spellingShingle Ke Pan
Ao Zeng
Xiaodie Ruan
Xinyu Mo
Bang Shen
Junlong Zhao
Yanqin Zhou
The apicoplast localized isocitrate dehydrogenase is needed for de novo fatty acid synthesis in the apicoplast of Toxoplasma gondii
Frontiers in Cellular and Infection Microbiology
Toxoplasma gondii
apicoplast
isocitrate dehydrogensase
metabolism
FAS 2
title The apicoplast localized isocitrate dehydrogenase is needed for de novo fatty acid synthesis in the apicoplast of Toxoplasma gondii
title_full The apicoplast localized isocitrate dehydrogenase is needed for de novo fatty acid synthesis in the apicoplast of Toxoplasma gondii
title_fullStr The apicoplast localized isocitrate dehydrogenase is needed for de novo fatty acid synthesis in the apicoplast of Toxoplasma gondii
title_full_unstemmed The apicoplast localized isocitrate dehydrogenase is needed for de novo fatty acid synthesis in the apicoplast of Toxoplasma gondii
title_short The apicoplast localized isocitrate dehydrogenase is needed for de novo fatty acid synthesis in the apicoplast of Toxoplasma gondii
title_sort apicoplast localized isocitrate dehydrogenase is needed for de novo fatty acid synthesis in the apicoplast of toxoplasma gondii
topic Toxoplasma gondii
apicoplast
isocitrate dehydrogensase
metabolism
FAS 2
url https://www.frontiersin.org/articles/10.3389/fcimb.2025.1542122/full
work_keys_str_mv AT kepan theapicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT aozeng theapicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT xiaodieruan theapicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT xinyumo theapicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT bangshen theapicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT junlongzhao theapicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT yanqinzhou theapicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT kepan apicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT aozeng apicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT xiaodieruan apicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT xinyumo apicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT bangshen apicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT junlongzhao apicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii
AT yanqinzhou apicoplastlocalizedisocitratedehydrogenaseisneededfordenovofattyacidsynthesisintheapicoplastoftoxoplasmagondii