Mutation in a light-regulated glucan synthase-like gene (gsl12) displays light hyper-responsive and callose deficient phenotypes in arabidopsis

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2009-05-15

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Light is a very important factor affecting every aspect of plant development. Plant developmental responses to light are sensitive to the direction, intensity, color, and duration of light. Light is perceived by an extensive set of photoreceptors that includes the red/far-red light?absorbing phytochromes and blue/UV-A light?absorbing cryptochromes. The Arabidopsis mutant seedling hyper-responsive to light 6 (shl6) has exaggerated developmental responses to available light. In the low light, shl6 seedlings have a phenotype similar to wild-type plants grown in high light, with short hypocotyls, expanded cotyledons, and well-developed first true leaves. In addition, the roots of shl6 are short and highly branched. The SHL6 gene was mapped to a position on chromosome 5 between simple sequence length polymorphism (SSLP) markers nga249 and nga151. Two cosmid clones from this interval (introduced by Agrobacterium-mediated transformation) complemented the shl6 mutant phenotype. One candidate gene identified by complementation is a member of the glycosyltransferase family. The sequence of shl6 mutant differs from wild type Columbia allele of this gene (At5g13000) by a single nucleotide substitution in the first exon. This putative SHL6 gene encodes a member of a glycan synthase-like (GSL12) gene family that includes callose synthase. The ?-1,3-D-glucan callose is found in the cell plate of dividing cells, in pollen mother cell walls, and pollen tubes. Callose synthase and related genes have not been previously implicated in developmental responses to light. We also observed that 90% of Col-0 anthers showed high callose deposition, but shl6 mutant did not display callose deposition in the anthers. The pollen viability in the shl6 was lower than Col-0. The epidermal cell elongation in shl6 hypocotyls was reduced when compared with Col-0. Therefore, we conclude that the mutation in light-regulated SHL6/GSL12 was involved in the synthesis of callose as well as light signaling.

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