bioRxiv Science⌕ Search

Biology subjects

Jorge, G. L.

Publications and source records attributed to Jorge, G. L..

3 recordsLinked to original sources

PII interactions with BADC and BCCP proteins co-regulate lipid and nitrogen metabolism in Arabidopsis

In plants the initiation of fatty acid synthesis is catalyzed by acetyl-CoA carboxylase (ACCase) which produces malonyl-CoA. The heteromeric form of ACCase (htACCase) is a holoenzyme consisting of biotin carboxylase and carboxyltransferase sub-complexes, both of which are subject to extensive regulation. Biotin carboxylase activity is controlled in part by the presence of the catalytic biotin carboxyl carrier proteins (BCCP1/2) and/or the non-catalytic, non-biotinylated, biotin/lipoyl attachment domain-containing proteins (BADC1/2/3) that associate with backbone biotin carboxylase (BC) protein. However, the mechanisms regulating BADC and BCCP interaction with BC and thus ACCase activity in planta are not clear. Here we demonstrate the Arabidopsis thaliana regulatory protein PII modulates htACCase activity through independent interactions with BADC and BCCP proteins in a selective manner. Analysis of badc1/2 and badc1/3 mutant lines and the respective pii triple mutants reveal that changes in seed oil and protein accumulation of badc double mutants are PII/nitrogen dependent. Absolute quantification of htACCase subunits and PII in developing seeds suggests that Arabidopsis exerts tight regulation over individual protein stoichiometry to balance oil and protein accumulation. The effects on vegetative and seed development indicate PII and BADC proteins have distinct but overlapping roles in the regulation of plant metabolism.

plant biology↗

Knocking out the carboxyltransferase interactor 1 (CTI1) in Chlamydomonas boosted oil content by fivefold without affecting cell growth

The first step in chloroplast de novo fatty acid synthesis is catalyzed by acetyl-CoA carboxylase (ACCase). As the rate-limiting step for this pathway, ACCase is subject to both positive and negative regulation. In this study, we identify a Chlamydomonas homolog of the plant carboxyltransferase interactor 1 (CrCTI1) and show that this protein, interacts with the Chlamydomonas -carboxyltransferase (Cr-CT) subunit of the ACCase by yeast two-hybrid protein-protein interaction assay. Three independent CRISPR-Cas9 mediated knock-out mutants for CrCTI1 each produced an "enhanced oil" phenotype, accumulating 25% more total fatty acids and storing up to five-fold more triacylglycerols (TAGs) in lipid droplets. The TAG phenotype of the crcti1 mutants was not influenced by light but was affected by trophic growth conditions. By growing cells under heterotrophic conditions, we observed a crucial function of CrCTI1 in balancing lipid accumulation and cell growth. Mutating a previously mapped in vivo phosphorylation site (CrCTI1 Ser108 to either Ala or to Asp), did not affect the interaction with Cr-CT. However, mutating all six predicted phosphorylation sites within Cr-CT to create a phosphomimetic mutant reduced significantly this pairwise interaction. Comparative proteomic analyses of the crcti1 mutants and WT suggested a role for CrCTI1 in regulating carbon flux by coordinating carbon metabolism, antioxidant and fatty acid {beta}-oxidation pathways, to enable cells adapt to carbon availability. Taken together, this study identifies CrCTI1 as a negative regulator of fatty acid synthesis in algae and provides a new molecular brick for genetic engineering of microalgae for biotechnology purposes.

plant biology↗

DYRKP kinase regulates cell wall degradation in Chlamydomonas by inducing matrix metalloproteinase expression

The cell wall of plants and algae is an important cell structure that protects cells from changes in the external physical and chemical environment. This extracellular matrix composed of polysaccharides and glycoproteins, is needed to be remodeled continuously throughout the life cycle. However, compared to matrix polysaccharides, little is known about the mechanisms regulating the formation and degradation of matrix glycoproteins. We report here that a plant kinase belonging to the dual-specificity tyrosine phosphorylation-regulated kinase (DYRK) family present in all eukaryotes regulates cell wall degradation in the model microalga Chlamydomonas reinhardtii by inducing the expression of matrix metalloproteinases (MMPs). In the absence of DYRKP, daughter cells fail to degrade the parental cell wall, and form multicellular structures. On the other hand, the complementation line of DYRKP was shown to degrade the parental cell wall normally. Transcriptomic and proteomic analyses indicate a marked down-regulation of MMP expression in the dyrkp mutants. Additionally, the expression of MMP was confirmed to be consistent with the expression pattern of DYRKP. Our findings show that DYRKP, by ensuring timely MMP expression, enables the successful execution of the cell cycle. Altogether, this study provides new insight into the life cycle regulation in plants and algae. IN A NUTSHELLO_ST_ABSBackgroundC_ST_ABSPlants and algae have different types of polysaccharides in their cell walls, but they have glycoproteins in common. Glycoprotein synthesis and degradation must be tightly regulated to ensure normal growth and differentiation. However, little is known about the regulatory mechanism of glycoprotein degradation in both plants and algae. The cell cycle of Chlamydomonas reinhardtii begins anew with the hatching of daughter cells, and the role of matrix metalloproteinases (MMPs) is known to be important in this process. In our previous study, we observed that a knockout mutant of the plant kinase belonging to the dual-specificity tyrosine phosphorylation-regulated kinase (DYRKP) formed a palmelloid structure and failed to hatch. QuestionsWhat is the role of DYRKP in microalgae? Specifically, why does the dyrkp mutant form a palmelloid structure? Palmelloid is usually observed in dividing cells or after exposure to stresses. We therefore hypothesized that the palmelloid phenotype observed in dyrkp mutant could either be due to a defect in cell hatching or due to an increased stress state in the mutant population. FindingsWe answered these questions by comparative studies in different culture conditions and by examining additional dyrkp knockout mutants generated by CRISPR-Cas9 in various background strains with more or less intact cell walls. Palmelloid formation in the dyrkp mutant was observed under optimal growth (mixo- or auto-trophic condition) and very low light conditions. Interestingly, unlike the parent strain, in which only cell wall fragments are observed in old cultures, the parental cell wall of the dyrkp mutant remained almost intact even after the release of daughter cells. Also, the cell division rate of the cell wall-less dyrkp mutants was similar to their background strain. These results suggest that dyrkp mutants have a problem in degrading the parental cell walls. Indeed, proteomic and transcriptomic analyses revealed reduced levels of protease families in the dyrkp mutant, and in particular with a significantly lower amount of several key members of the MMP family. Through the analysis of complementation lines, we confirmed that the DYRKP was required for strong and rapid expression of MMPs. Next stepsWe are pursuing research to understand what the phosphorylation clients of DYRKP are and how they regulate the expression of the MMPs identified in this study. One sentence summaryThe DYRKP kinase induces the expression of matrix metalloproteinases involved in the degradation of the parental cell wall, allowing prompt hatching of daughter cells after cell division.

plant biology↗