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Results 1 - 10 of 31 > >>
EC Number General Information Commentary Reference
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction a stearoyl-acyl carrier protein fatty acid desaturase mutant has decreased lateral root growth due to a defect in the cell elongation 728530
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction downregulation of ZmSAD1 increases the stearic acid concentration in maize leaf 746527
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction fatty acid composition of wild-type and mutant plants, overview 746135
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction one nonsense and four missense Gmsacpd-c mutants are identified to have high levels of seed, nodule, and leaf stearic acid content. Homology modeling and in silico analysis of the GmSACPD-C enzyme reveals that most of these mutations are localized near or at conserved residues essential for di-iron ion coordination. Soybeans carrying Gmsacpd-c mutations at conserved residues cause the highest stearic acid content, and these mutations have deleterious effects on nodule development and function. Mutant plants with mutations at nonconserved residues show an increase in stearic acid content yet retain healthy nodules. Nodule leg hemoglobin transcripts are significantly more abundant in soybeans with deleterious mutations at conserved residues of GmSACPD-C. Gmsacpd-c mutations cause an increase in leaf stearic acid content and an alteration of leaf structure and morphology in addition to differences in nitrogen-fixing nodule structure. Wild-type and mutant leaf phenotypes, overview 746120
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction Ophrys SAD coding sequences are heterologously expressed in Arabidopsis under the control of the Cauliflower mosaic virus 35S RNA promoter. None of the transgenic plant lines complement the dwarf phenotype of homozygous ssi2 mutants. The presence of the OsSAD2 transgene is significantly associated with changes in unsaturated C18 and C16 FA levels in Arabidopsis leaf lipids, suggesting that OsSAD2 has enzymatic activity in Arabidopsis 713432
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction Ophrys SAD coding sequences are heterologously expressed in Arabidopsis under the control of the Cauliflower mosaic virus 35S RNA promoter. OeSAD2 does not complement the dwarf phenotype of homozygous ssi2 mutants 713432
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction Ophrys SAD coding sequences are heterologously expressed in Arabidopsis under the control of the Cauliflower mosaic virus 35S RNA promoter. OsSAD1 does not complement the dwarf phenotype of homozygous ssi2 mutants 713432
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction seed homozygous for the SACPD-C deletion averages 10.4% stearic acid and 75.9% oleic acid 728825
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction the isozyme A-C triple knockdown plants display severe growth phenotypes, including spontaneous cell death and dwarfing. While no vegetative morphologic abnormality is observed in individual NbSACPD-A, -B, or -C knockdown plants, strikingly, NbSACPD-C knockdown plants produce small fruits with aborted ovules. Reciprocal crosses with wild-type and NbSACPD-C knockdown plants reveal that knocking down NbSACPD-C expression causes female, but not male, sterility. Arrested ovule development and significantly altered lipid composition in ovaries are observed in NbSACPD-C knockdown plants, consistent with the predominant NbSACPD-C expression in ovules. The ovule development defect is fully complemented by coexpressing an amiRNA-resistant NbSACPD-C variant in the NbSACPD-C knockdown background, further supporting a specific requirement for NbSACPD-C in female fertility. Phenotypes, overview 746079
Show all pathways known for 1.14.19.2Display the word mapDisplay the reaction diagram Show all sequences 1.14.19.2malfunction the isozyme A-C triple knockdown plants display severe growth phenotypes, including spontaneous cell death and dwarfing. While no vegetative morphologic abnormality is observed in individual NbSACPD-A, -B, or -C knockdown plants, strikingly, NbSACPD-C knockdown plants show a highly altered phenotype, overview. Phenotypes, overview 746079
Results 1 - 10 of 31 > >>