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    Online-Ressource
    Online-Ressource
    Proceedings of the National Academy of Sciences ; 2019
    In:  Proceedings of the National Academy of Sciences Vol. 116, No. 41 ( 2019-10-08), p. 20776-20785
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 116, No. 41 ( 2019-10-08), p. 20776-20785
    Kurzfassung: sugary enhancer1 ( se1 ) is a naturally occurring mutant allele involved in starch metabolism in maize endosperm. It is a recessive modifier of sugary1 ( su1 ) and commercially important in modern sweet corn breeding, but its molecular identity and mode of action remain unknown. Here, we developed a pair of near-isogenic lines, W822Gse ( su1-ref/su1-ref se1/se1 ) and W822GSe ( su1-ref/su1-ref Se1/Se1 ), that Mendelize the se1 phenotype in an su1-ref background. W822Gse kernels have lower starch and higher water soluble polysaccharide and sugars than W822GSe kernels. Using high-resolution genetic mapping, we found that wild-type Se1 is a gene Zm00001d007657 on chromosome 2 and a deletion of this gene causes the se1 phenotype. Comparative metabolic profiling of seed tissue between these 2 isolines revealed the remarkable difference in carbohydrate metabolism, with sucrose and maltose highly accumulated in the mutant. Se1 is predominantly expressed in the endosperm, with low expression in leaf and root tissues. Differential expression analysis identified genes enriched in both starch biosynthesis and degradation processes, indicating a pleiotropic regulatory effect of se1 . Repressed expression of Se1 and Su1 in RNA interference-mediated transgenic maize validates that deletion of the gene identified as Se1 is a true causal gene responsible for the se1 phenotype. The findings contribute to our understanding of starch metabolism in cereal crops.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 2019
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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