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ROUGH SHEATH2: A Myb Protein That Represses knox Homeobox Genes in Maize Lateral Organ Primordia

Authors: Marja C. P.; null Timmermans; Andrew Hudson; Philip W. Becraft; Timothy Nelson;

ROUGH SHEATH2: A Myb Protein That Represses knox Homeobox Genes in Maize Lateral Organ Primordia

Abstract

The regulation of members of the knotted1 -like homeobox ( knox ) gene family is required for the normal initiation and development of lateral organs. The maize rough sheath2 ( rs2 ) gene, which encodes a Myb-domain protein, is expressed in lateral organ primordia and their initials. Mutations in the rs2 gene permit ectopic expression of knox genes in leaf and floral primordia, causing a variety of developmental defects. Ectopic KNOX protein accumulation in rs2 mutants occurs in a subset of the normal rs2 -expressing cells. This variegated accumulation of KNOX proteins in rs2 mutants suggests that rs2 represses knox expression through epigenetic means.

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Keywords

Homeodomain Proteins, Meristem, Molecular Sequence Data, Genes, Homeobox, Down-Regulation, Genes, Plant, Zea mays, DNA-Binding Proteins, Plant Leaves, Repressor Proteins, Proto-Oncogene Proteins c-myb, Gene Expression Regulation, Plant, Mutation, Amino Acid Sequence, Sequence Alignment, Plant Proteins

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Powered by OpenAIRE graph
citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
292
Top 1%
Top 1%
Top 1%