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Procuste1 mutants identify two distinct genetic pathways controlling hypocotyl cell elongation, respectively in dark and light-grown Arabidopsis seedlings
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1996 (English)In: Development, ISSN 0950-1991, E-ISSN 1477-9129, Vol. 122, no 2, 683-693 p.Article in journal (Refereed) PublishedText
Abstract [en]

Plant morphogenesis is dependent on a tight control of cell division and expansion. Cell elongation during postembryonic hypocotyl growth is under the control of a light-regulated developmental switch. Light is generally believed to exert its effects on hypocotyl elongation through a phytochrome- and blue-light receptor- mediated inhibitory action on a so far unknown cell elongation mechanism. We describe here a new class of allelic mutants in Arabidopsis, at the locus PROCUSTE1 (prc1-1 to -4), which have a hypocotyl elongation defect specifically associated with the dark-grown developmental program. Normal hypocotyl elongation is restored in plants grown in white, blue or red light. In agreement with this, the constitutive photomorphogenic mutation cop1-6, which induces a deetiolated phenotype in the dark, is epistatic to prc1-2 for the hypocotyl phenotype. Epistasis analyses in red and blue light respectively, indicate that phytochrome B but not the blue light receptor HY4, is required for the switch from PRC1-dependent to PRC1-independent elongation. The conditional hypocotyl growth defect is associated with a deformation of the hypocotyl surface due to an uncontrolled swelling of epidermal, cortical or endodermal cells, suggesting a defect in the structure of the expanding cell wall, A similar phenotype was observed in elongating roots, which was however, independent of the light conditions. The aerial part of mature mutant plants grown in the light was indistinguishable from the wild type. prc1 mutants provide a means of distinguishing, for the first time, two genetic pathways regulating hypocotyl cell elongation respectively in dark- and light-grown seedlings, whereby light not only inhibits hypocotyl growth, but also activates a PRC1-independent cell elongation program.

Place, publisher, year, edition, pages
1996. Vol. 122, no 2, 683-693 p.
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Natural Sciences
URN: urn:nbn:se:umu:diva-114198OAI: diva2:914089

Times Cited: 73 75

Available from: 2016-03-23 Created: 2016-01-15 Last updated: 2016-03-23

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Bellini, C.
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