Linked Life Data

1995419

Source:http://linkedlifedata.com/resource/pubmed/id/1995419

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-3-22
pubmed:abstractText
Genes encoding fusions between the maize regulatory protein C1 and the yeast transcriptional activator GAL4 and mutant C1 proteins were assayed for their ability to trans-activate anthocyanin biosynthetic genes in intact maize tissues. The putative DNA-binding region of C1 fused to the transcriptional activation domain of GAL4 activated transcription of anthocyanin structural gene promoters in c1 aleurones, c1 Rscm2 embryos, and c1 r embryogenic callus. Cells receiving these constructs accumulated purple anthocyanin pigments. The C1 acidic region fused to the GAL4 DNA-binding domain activated transcription of a GAL4-regulated promoter. An internal deletion of C1 also induced pigmentation; however, frameshifts in either the amino-terminal basic or carboxy-terminal acidic region blocked trans-activation, and the latter generated a dominant inhibitory protein. Fusion constructs between the wild-type C1 cDNA and the dominant inhibitor allele C1-I cDNA were used to identify the amino acid changes in C1 responsible for the C1-I inhibitory phenotype. Results from these studies establish that amino acids within the myb-homologous domain are critical for transcriptional activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0890-9369
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
298-309
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Identification of functional domains in the maize transcriptional activator C1: comparison of wild-type and dominant inhibitor proteins.
pubmed:affiliation
U.S. Department of Agriculture/University of California, Berkeley, Albany 94710.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.