Expression Of Fatty Acid Biosynthetic Genes Research Articles

TEOSINTE BRANCHED1/CYCLOIDEA/PROLIFERATING CELL FACTOR4 Interacts with WRINKLED1 to Mediate Seed Oil Biosynthesis.

Cross-family transcription factor (TF) interactions play critical roles in the regulation of plant developmental and metabolic pathways. WRINKLED1 (WRI1) is a key TF governing oil biosynthesis in plants. However, little is known about WRI1-interacting factors and their roles in oil biosynthesis. We screened a TF library using Arabidopsis (Arabidopsis thaliana) WRI1 (AtWRI1) as bait in yeast two-hybrid assays and identified three TEOSINTE BRANCHED1/CYCLOIDEA/PROLIFERATING CELL FACTOR (TCP) family TFs, namely TCP4, TCP10, and TCP24, as AtWRI1-interacting partners. The physical interaction between AtWRI1 and TCPs was further validated using bimolecular fluorescence complementation assays. TCPs play important roles in various plant developmental processes; however, their involvement in fatty acid biosynthesis was not previously known. Coexpression of TCP4, but not TCP10 or TCP24, with AtWRI1 reduced AtWRI1-mediated oil biosynthesis in Nicotiana benthamiana leaves. Transcriptomic analysis in transgenic Arabidopsis plants with enhanced TCP4 activity engineered by expressing rTCP4 (i.e. miR319-resistant TCP4) revealed that AtWRI1 target genes were significantly repressed. TCP4 expression is strongly correlated with AtWRI1 during embryo development. A tcp4 loss-of-function mutant, the jaw-D mutant with a strong reduction of TCP4 expression, and a tcp2 tcp4 tcp10 triple mutant accumulated more seed oil than wild-type Arabidopsis. In addition, TCP4 repressed the AtWRI1-mediated transactivation of the promoters of fatty acid biosynthetic genes. Collectively, our findings suggest that TCP4 represses fatty acid biosynthetic gene expression through interaction with AtWRI1, leading to a reduction of AtWRI1-mediated seed oil accumulation.

Elucidating the role of jasmonic acid in oil accumulation, fatty acid composition and gene expression in Chlorella vulgaris (Trebouxiophyceae) during early stationary growth phase

Manipulation of microalgae cultivation is an important approach as the growth conditions will determine the quality and compositions of lipids produced by the cells. This study attempts at maximizing the production of lipids in Chlorella vulgaris (Trebouxiophyceae) through introduction of the plant hormone jasmonic acid (JA). Exogenous application of JA at early stationary growth phase promoted microalgal growth with increment of up to 51% of cell density relative to the control. JA also transiently increased the total oil production of microalgal cells by 54%. Interestingly, this increment also induced significantly higher production of saturated (SFA) and monounsaturated (MUFA) without compensating the production of polyunsaturated fatty acid (PUFA). Further analysis of fatty acid compositions showed that JA stimulated the production of C16:0 (palmitic acid), C18:0 (stearic acid) and C18:1 (oleic acid) at early stationary growth phase whilst C18:3 n-3 (α-linolenic acid) at later stationary growth phase. This transient modification of fatty acid compositions was correlated with the fatty acid biosynthetic gene expression as quantified by real-time PCR. Taken together, our results indicated that JA significantly increased microalgal lipid accumulation and could be utilized in cultivation to facilitate commercial mass production of microalgae lipids.

Developmental control of Arabidopsis seed oil biosynthesis

Arabidopsis transcriptional factors LEAFY COTYLEDON1 (LEC1), LEAFY COTYLEDON2 (LEC2), FUSCA3 (FUS3), ABSCISIC ACID3 (ABI3), and ABSCISIC ACID5 (ABI5) are known to regulate multiple aspects of seed development. In an attempt to understand the developmental control of storage product accumulation, we observed the expression time course of the five transcripts. The sequential expression of these factors during seed fill suggests differentiation of their normal responsibilities. By extending the expression periods of the two early genes LEC1 and LEC2 in transgenic seeds, we demonstrated that the subsequent timing of FUS3, ABI3, and ABI5 transcripts depends on LEC1 and LEC2. Because a delayed onset or reduced level of FUS3 mRNA coincided with reduction of seed oil content in the transgenic seeds, the role of FUS3 in oil deposition was further examined. Analysis of published seed transcriptome data indicated that FUS3 transcript increased together with nearly all the plastidial fatty acid biosynthetic transcripts during development. The ability of FUS3 to rapidly induce fatty acid biosynthetic gene expression was confirmed using transgenic Arabidopsis seedlings expressing a dexamethasone (DEX)-inducible FUS3 and Arabidopsis mesophyll protoplasts transiently expressing the FUS3 gene. By accommodating the current evidence, we propose a hierarchical architecture of the transcriptional network in Arabidopsis seeds in which the oil biosynthetic pathway is integrated through the master transcriptional factor FUS3.

An integrative metabolism approach identifies stearoyl‐CoA desaturase as a target for an arachidonate‐enriched diet

Epidemiological studies have correlated diets containing higher intakes of PUFA with lower rates of chronic metabolic diseases. The molecular mechanisms regulated by the consumption of PUFA were examined by using an integrative metabolism approach assaying the liver transcriptome and lipid-metabolome of mice fed a control diet, an arachidonate (AA)-enriched fungal oil, an eicosapentaenoic (EPA)/docosahexaenoic (DHA)-enriched fish oil, or a combination of the two oils. Hepatic gene transcription and fatty acid (FA) metabolism were significantly altered by diets enriched with AA, as revealed by global error assessment and singular value decomposition (SVD) analysis, respectively. SVD analysis of the lipid data, reinforced with transcriptomics, suggests that the chronic feeding of AA modulates molecular endpoints similar to those previously reported in the obesity-resistant SCD1-/- mouse, namely, genes involved in lipid oxidation/synthesis and the significant changes in FA metabolism stemming from a repressed SCD1 activity. Specifically, the total levels and FA composition of several phospholipid (PL) species were significantly changed, with phosphatidylcholine (PC) demonstrating the greatest alterations. Reduced PC levels were linked to decreased expression of enzymes in PC biosynthesis (choline kinase, -2.2-fold; glycerol-3-phosphate acyltransferase, -2.0-fold). Alterations in PL-FA composition were related to decreased expression of FA biosynthetic genes [fatty acid synthetase, -3.7-fold; stearoyl-CoA desaturase-1 (SCD1), -1.8-fold]. Lower hepatic SCD1 gene expression levels were reflected in various aspects of FA metabolism through increased concentrations of palmitic (fungal oil, +45%; combination, +106%) and stearic acids (fungal oil, +60%; combination, +63%) in PC. Importantly, an integrated approach showed that these effects were not attenuated by the addition of an EPA/DHA-enriched fish oil, thereby identifying a previously unrecognized and distinct role for AA in the regulation of hepatic lipid metabolism.