Abstract
BackgroundIn part due to the ease of visual detection of phenotypic changes, anthocyanin pigment production has long been the target of genetic and molecular research in plants. Specific members of the large family of plant myb transcription factors have been found to play critical roles in regulating expression of anthocyanin biosynthetic genes and these genes continue to serve as important tools in dissecting the molecular mechanisms of plant gene regulation.FindingsA spontaneous mutation within the coding region of an Arabidopsis 35S::AtMYB90 transgene converted the activator of plant-wide anthocyanin production to a dominant-negative allele (PG-1) that inhibits normal pigment production within tobacco petals. Sequence analysis identified a single base change that created a premature nonsense codon, truncating the encoded myb protein. The resulting mutant protein lacks 78 amino acids from the wild type C-terminus and was confirmed as the source of the white-flower phenotype. A putative tobacco homolog of AtMYB90 (NtAN2) was isolated and found to be expressed in flower petals but not leaves of all tobacco plants tested. Using transgenic tobacco constitutively expressing the NtAN2 gene confirmed the NtAN2 protein as the likely target of PG-1-based inhibition of tobacco pigment production.ConclusionsMessenger RNA and anthocyanin analysis of PG-1Sh transgenic lines (and PG-1Sh x purple 35S::NtAN2 seedlings) support a model in which the mutant myb transgene product acts as a competitive inhibitor of the native tobacco NtAN2 protein. This finding is important to researchers in the field of plant transcription factor analysis, representing a potential outcome for experiments analyzing in vivo protein function in test transgenic systems that over-express or mutate plant transcription factors.
Highlights
Anthocyanins represent a broad family of plant pigments that contribute to flower and fruit pigmentation [1], plant stress response [2,3] and have been implicated as helpful nutrients that contribute to improved human health [4]
Messenger RNA and anthocyanin analysis of PG-1Sh transgenic lines support a model in which the mutant myb transgene product acts as a competitive inhibitor of the native tobacco NtAN2 protein
This finding is important to researchers in the field of plant transcription factor analysis, representing a potential outcome for experiments analyzing in vivo protein function in test transgenic systems that overexpress or mutate plant transcription factors
Summary
Anthocyanins represent a broad family of plant pigments that contribute to flower and fruit pigmentation [1], plant stress response [2,3] and have been implicated as helpful nutrients that contribute to improved human health [4]. A classic example of this form of gene regulation was originally identified through genetic mapping of maize mutations affecting seed-coat color. Many of these maize mutant alleles mapped to the C1 (MYB) [14,15], R (bHLH) [16,17], or PAC1 (WD40) [18] loci [19]. Other examples of plant MYB genes in the R2R3 family [20,21] have been found to play significant roles in controlling pigment production in flowers, fruit and vegetative tissues of several plant species [9,22]. Specific members of the large family of plant myb transcription factors have been found to play critical roles in regulating expression of anthocyanin biosynthetic genes and these genes continue to serve as important tools in dissecting the molecular mechanisms of plant gene regulation
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