Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Mar 3;35(6):1984–2005. doi: 10.1093/plcell/koad059

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2023. Published by Oxford University Press on behalf of American Society of Plant Biologists.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

PMC Copyright notice

Figure 8. — Model summarizing the role of KCS4 on FA fate in Arabidopsis under carbon starvation. The lack of de novo FA synthesis under heat and darkness (HD) or extended darkness (3D, 6D) induces the degradation of galactolipids (MGDGs and DGDGs) from the chloroplasts’ thylakoids. FFAs are then exported to the ER (FA-CoA pool), where KCS4 is localized and acts as a branch point in the fate of FAs, channeling saturated FAs to VLCFA elongation and tipping the balance to a higher polyunsaturated-to-saturated-FA ratio for puTAG accumulation (degrade grey arrows). Two KCS4 alleles have differential capacity to allocate saturated FAs into the VLCFA pathway, with a major -more efficient- allele, KCS4(Met), and a minor -weaker allele, KCS4(Thr), exemplified here in different sizes. KCS4(Met) accessions efficiently channel the saturated FA from the Acyl-CoA pool to cuticular waxes, as they present higher accumulation of waxes than KCS4(Thr) accessions under stress. In addition, polyunsaturated TAG (puTAGs) levels are, therefore, higher in KCS4(Met) accessions compared to KCS4(Thr) accessions, as the result of a rise in the ratio of polyunsaturated-to-saturated FAs going to TAG formation. VLCFA-CoA produced by the elongase complex (here exemplified by KCS4, KCR, HCD, ECR) go to increase the cuticular waxes under HD and/or directly serve as a source of carbon undergoing degradation in the peroxisome; whereas puTAGs accumulate into lipid bodies first. FFAs are then released from lipid bodies by the action of lipases (SDP1) and further imported to the peroxisome to undergo β-oxidation. Acronyms: ABCA9 (ATP-BINDING CASSETTE A9; AT5G61730), ACBP-1 (Acyl-CoA-binding protein 1; AT5G53470); ACX (ACYL-COA OXIDASE); CoA (coenzyme A); DGDG (digalactosyldiacylglycerol); ECR (ENOYL-COA REDUCTASE; AT3G55360); FAs (fatty acids); FAS (fatty acid synthesis); FAX1 (FATTY ACID EXPORT1; AT3G57280); FFAs (free fatty acids); HCD (β-HYDROXYACYL-COA DEHYDRATASE); IAA (indol-3-acetic-acid), IBA (indol-3-butyric-acid), KCR (β-KETOACYL REDUCTASE); KCS4(Met/Thr) (3-KETOACYL-COA SYNTHASE4); LACS (LONG-CHAIN ACYL-COA SYNTHETASE); SDP1 (SUGAR DEPENDENT1; AT5G04040); MGDG (monogalactosyldiacylglycerol); PXA1 (PEROXISOMAL ABC-TRANSPORTER 1; AT4G39850); pu (polyunsaturated), sa (saturated), TAGs (triacylglycerols); VLCFA (very long chain fatty acid).