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Deborah Long

Researcher at John Innes Centre

Publications -  9
Citations -  1752

Deborah Long is an academic researcher from John Innes Centre. The author has contributed to research in topics: Arabidopsis & Mutant. The author has an hindex of 9, co-authored 9 publications receiving 1698 citations. Previous affiliations of Deborah Long include Norwich Research Park.

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A Polycomb-group gene regulates homeotic gene expression in Arabidopsis

TL;DR: It is shown here that the CURLY LEAF gene of Arabidopsis is necessary for stable repression of a floral homeotic gene and encodes a protein with homology to the product of the Polycomb-group gene Enhancer of zeste.
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ACAULIS5, an Arabidopsis gene required for stem elongation, encodes a spermine synthase.

TL;DR: The results of the experiments showed that polyamines play an essential role in promotion of internode elongation through cell expansion in Arabidopsis and the relationships to plant growth regulators such as auxin and gibberellins that have related functions.
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A Dissociation insertion causes a semidominant mutation that increases expression of TINY, an Arabidopsis gene related to APETALA2.

TL;DR: A transposon-tagging strategy designed to recover dominant gain-of-function alleles was performed with Arabidopsis by using a Dissociation element with a cauliflower mosaic virus 35S promoter transcribing outward over one terminus as discussed by the authors.

A Dissociation Insertion Causes a Semidominant Mutation That Increases Expression of TINY, an Arabidopsis Gene

TL;DR: A novel transposon-tagging strategy designed to recover dominant gain-of-function alleles was performed with Arabidopsis by using a Dissociation element with a cauliflower mosaic virus 35S promoter transcribing outward over one terminus, resulting in a semidominant mutation affecting plant height, hypocotyl elongation, and fertility.
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Mutation of a family 8 glycosyltransferase gene alters cell wall carbohydrate composition and causes a humidity-sensitive semi-sterile dwarf phenotype in Arabidopsis.

TL;DR: Cell-wall carbohydrate analyses of the parvus mutant indicated reduced levels of rhamnogalacturonan I branching and alterations in the abundance of some xyloglucan linkages that may, however, be indirect consequences of the mutation.