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EC Number
General Information
Commentary
Reference
evolution
phylogeny of the YL-1 protein family, overview
evolution
the enzyme belongs to the ferritin-like, diiron-carboxylate protein family
malfunction
a Chl27-antisense Arabidopsis mutant accumulates the cyclase substrate magnesium-protoporphyrin IX monomethyl ester and does not produce protochlorophyllide a
malfunction
a Rubrivivax gelatinosus strain with disrupted acsF gene cannot synthesize bacteriochlorophyll under oxygenated conditions but accumulates the substrate magnesium-protoporphyrin IX monomethyl ester, in contrast, under low-oxygene conditions the phenotype is similar to the wild-type, an alternative pathway for the reaction exists vie the bchE genes
malfunction
chlorophyll biosynthesis upstream genes are highly expressed in the yl-1 mutant, while downstream genes are compromised, indicating that enzyme MPEC plays a pivotal role in the chlorophyll biosynthesis. The yl-1 mutant shows a yellow leaf and panicle phenotype with reduced chlorophyll accumulation through the whole growth phases. Mutant yl-1 exhibits the temperature-independent yellow leaf phenotype, it presents abnormal chloroplast development and attenuated photosynthetic efficiency. The mutant yl-1 affects mRNA accumulation levels of Chl biosynthesis process
malfunction
crd1 strains fail to accumulate photosystem 1 (PS 1) and light-harvesting complex 1 (LHC 1) during hypoxia or copper deficiency, and have reduced amounts of LHC 2, Crd1 abundance is increased in copper or oxygen deficient cells; Cth1 accumulates in copper-sufficient, oxygenated cells
malfunction
decreased CHL27 transcript levels result in a substantial reduction of activity of MgPME cyclase and MgP monomethylester accumulation, in comparison to dexamethasone-treated wild-type seedlings
malfunction
deficiency of the LCAA subunit affects Ala synthesis and the accumulation of proteins in tetrapyrrole biosynthesis
malfunction
Hordeum vulgare mutants viridis-k, light green 3, light green 4 and zebra stripe 2 are not deficient in Ycf54. Both xanthan-l and viridis-k membranes are unable to support MPEC activity when combined with wild-type soluble fraction
malfunction
mutation of in enzyme MPEC causes the pale-green leaf mutant phenotype of mutant m167 with yellow-green leaves across the whole lifespan. Chlorophyll content decreases by 43-51% and the granal stacks of chloroplasts becomes thinner in m167. Chlorophyll fluorescence parameters, including Fv/Fm (the maximum quantum efficiency of PSII) and quantum yield of PSII (Y(II)), are lower in m167 than those in wild-type plants, and photosynthesis rate decreases by 40% in leaves of m167 mutant compared with wild-type plants, which leads to yield reduction in m167
Results 1 - 10 of 26 > >>