Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 10/20/2009
Publication Date: 2/24/2010
Citation: Velten, J.P., Cakir, C. 2010. A dominant-negative mutation within AtMYB90 blocks flower pigment production in transgenic tobacco [abstract]. Keystone Symposium: RNS Silencing Mechanisms in Plants.
Technical Abstract: During de novo shoot induction in cultured transgenic tobacco callus a spontaneous mutation within the coding region of a AtMYB90 transgene produced a plant line in which the original transgene-induced over-pigmented phenotype (dark red/purple from anthocyanin overproduction in most tissues) was lost. The mutation caused nearly all tissues to revert to their normal color, with the single exception being flower petals which, instead, displayed a dramatic reduction in pigment production when compared to wild-type tobacco. The white-flower-mutant transgene allele (PG-1) was found to be dominant-negative and to have resulted from a single base change within the AtMYB90 coding region, converting lysine-172 to a nonsense codon (AAG->TAG) and removing 78 amino acids from the C-terminus of the encoded protein (wild-type length = 249 AA). Comparison of gene-expression patterns of the PG-1 allele, it’s wild-type progenitor (Myb-27) and a flower-specific tobacco MYB-R2R3 putative homolog (NtMYB-141), supports a model in which the truncated PG-1 protein acts as a competitive inhibitor of the endogenous tobacco MYB transcription factor that controls flower color. The PG-1 phenotype is similar to that previously reported for tobacco plants that ectopically over-expressed either the maize CI-1 dominant-negative MYB mutant, or a wild-type heterologous MYB factor that controls anthocyanin production in strawberry fruit. Comparison of the predicted PGW protein to these, and other related anthocyanin regulatory MYB proteins, provides useful insight into the function of MYB-R2R3 transcription factors in regulating plant gene expression