Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.15 (pectinase)
 2,440 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We isolated a T-DNA-tagged mutant named hosoba toge toge (hot) in which a pleiotropic phenotype was observed in both the shoot and root throughout the life cycle. The phenotype and allelism indicated that the mutant has a defect in both the FASCIATA1 (FAS1) gene and the FT gene located on the bottom arm of chromosome 1. Analysis of the junctions between the T-DNA ends and the plant genome suggested the presence of a 75.8-kbp deletion at the insertion site. In addition to FAS1 and FT, 13 genes were predicted to exist in the region corresponding to that deleted in hot. They include homologs of genes for type II inositol-1,4,5-triphosphate 5-phosphatase (IP5Pase), the beta-chain of N-acetyl-beta-glucosaminidase (NAGase), NADPH oxidoreductase of the zeta-crystallin family, polygalacturonase, and endo-1,4-beta-glucanase. Although most aspects of the hot phenotype can be explained by loss of FAS1 and FT functions, some novel phenotypic features which may represent aspects of a mutant phenotype due to loss-of-function of other gene(s) were observed. One "wild-type" ecotype and a previously reported T-DNA insertion line, neither of which has any obvious phenotypic abnormality, carry a possible loss-of-function mutation in the zeta-crystallin homolog and in the NAGase beta chain homolog, respectively.
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PMID:hosoba toge toge, a syndrome caused by a large chromosomal deletion associated with a T-DNA insertion in Arabidopsis. 1110 Jul 78

Chloroplast biogenesis in angiosperm plants requires the light-dependent transition from an etioplast stage. A key factor in this process is NADPH:protochlorophyllide oxidoreductase A (PORA), which catalyzes the light-dependent reduction of protochlorophyllide to chlorophyllide. In a recent study the chloroplast outer envelope channel OEP16 was described to be involved in etioplast to chloroplast transition by forming the translocation pore for the precursor protein of PORA [Pollmann et al. (2007) Proc Natl Acad Sci USA 104:2019-2023]. This hypothesis was based on the finding that a single OEP16.1 knockout mutant in Arabidopsis thaliana was severely affected during seedling de-etiolation and PORA protein was absent in etioplasts. In contrast, in our study the identical T-DNA insertion line greened normally and showed normal etioplast to chloroplast transition, and mature PORA was present in etioplasts [Philippar et al. (2007) Proc Natl Acad Sci USA 104:678-683]. To address these conflicting results regarding the function of OEP16.1 for PORA import, we analyzed several lines segregating from the original OEP16.1 T-DNA insertion line. Thereby we can unequivocally show that the loss of OEP16.1 neither correlates with impaired PORA import nor causes the observed de-etiolation phenotype. Furthermore, we found that the mutant line contains at least 2 additional T-DNA insertions in the genes for the extracellular polygalacturonase converter AroGP1 and the plastid-localized chorismate mutase CM1. However, detailed examination of the de-etiolation phenotype and a genomewide transcriptional analysis revealed no direct influence of these genes on etioplast to chloroplast transition in Arabidopsis cotyledons.
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PMID:A search for factors influencing etioplast-chloroplast transition. 1956 34