Location: Plant Physiology and Genetics ResearchTitle: CGI-58 regulates triacylglycerol homeostasis and lipid signaling pathways in plants through interaction with the peroxisomal transport protein PXA1.) Author
Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 11/2/2012
Publication Date: N/A
Citation: Interpretive Summary:
Technical Abstract: Mutation of the Comparative Gene Identification-58 (CGI-58) gene in humans causes Chanarin-Dorfman syndrome, a rare genetic disorder characterized by an increase in triacylglycerol (TAG) and lipid droplet (LD) contents in non-lipid-storing cell types. Interestingly, disruption of the CGI-58 homologue in Arabidopsis causes a similar accumulation of TAG and LDs in non-lipid storing tissues (e.g., leaves and stems), suggesting that the molecular mechanism(s) underpinning CGI-58 activity might be conserved in plants and animals. Key proteins known to be important for modulating the activity of CGI-58 in mammals through protein-protein interaction, however, are absent in plants. To elucidate the function of CGI-58 in plants, we used Arabidopsis CGI-58 as bait in a yeast two-hybrid screen and identified PXA1 as an interacting protein. PXA1 is a peroxisomal membrane protein that transports both fatty acids and lipophilic hormones (e.g., 12-oxophytodienoic acid [OPDA] and indole-3-butyric acid [IBA]) into the peroxisome for subsequent breakdown or metabolic conversion to jasmonic acid (JA) and indole-3-acetic acid (IAA), respectively. Other experiments have shown that disruption of PXA1, like CGI-58, results in the abnormal accumulation of TAG and lipid droplets in vegetative cells types, suggesting that CGI-58 and PXA1 are functionally related. In support of this premise, cgi-58 mutant plants showed elevated accumulation of OPDA and reduced amounts of JA in response to plant wounding, similar to (but less severe than) pxa1 mutants. In addition, cgi-58 mutant plants were resistant to the effects of IBA (the peroxisomal precursor) in root elongation assays, but sensitive to IAA (the peroxisomal product). Unlike pxa1 mutants, however, cgi-58 mutant seeds can germinate and undergo seedling establish in the absence of exogenously provided sucrose. Collectively, these results indicate that CGI-58 and PXA1 function cooperatively in the regulation of fatty acid (and thus TAG) homeostasis in vegetative tissues, and also regulate a variety of lipid signaling pathways. Implications for the metabolic engineering of plants for enhanced oil production, as well as new insights to lipid metabolic disorders in humans, will be discussed.