Evolutionary divergence of LFY function in the mustards Arabidopsis thaliana and Leavenworthia crassa

• Published in: Plant molecular biology Vol. 62; no. 1-2; pp. 279 - 289
• Main Authors: Sliwinski, M.K, White, M.A, Maizel, A, Weigel, D, Baum, D.A
• Format: Journal Article
• Language: English
• Published: Netherlands Springer Nature B.V 01.09.2006
• Subjects: Arabidopsis - classification; Arabidopsis - genetics; Arabidopsis Proteins - genetics; Arabidopsis thaliana; Brassicaceae; DNA Primers; Evolution, Molecular; Flowers; Flowers & plants; Genes; Genetic Variation; Mustard Plant - classification; Mustard Plant - genetics; Plant Proteins - genetics; Proteins; Regulation; Reverse Transcriptase Polymerase Chain Reaction; Transcription Factors - genetics; Transcription, Genetic
• ISSN: 0167-4412; 1573-5028
• DOI: 10.1007/s11103-006-9020-3

LEAFY (LFY), a transcription factor involved in the regulation of flower development in Arabidopsis thaliana, has been identified as a candidate gene in the diversification of plant architecture in Brassicaceae. Previous research with Leavenworthia crassa, which produces solitary flowers in the axils of rosette leaves, has shown that the L. crassa LFY ortholog, LcrLFY, rescues most aspects of flower development in A. thaliana but showed two novel traits: flowers produced additional petals and inflorescences produced terminal flowers. In this paper, we explore the molecular mechanisms responsible for these novel phenotypes. We used microarray hybridizations to identify 32 genes differentially expressed between a transgenic LcrLFY line and a control transgenic LFY line. Of particular interest, TERMINAL FLOWER 1 (TFL1) transcripts were found at elevated levels in LcrLFY lines. To distinguish regulatory versus functional changes within the LcrLFY locus, reciprocal chimeric transgenes between LcrLFY and LFY were constructed. These lines implicate divergence of LcrLFY cis-regulation as the primary cause of both novel transgenic phenotypes but implicate divergence of LcrLFY protein function as the primary cause of elevated TFL1 levels. Taken together these results show that LcrLFY has diverged from A. thaliana in both the cis-regulatory and protein-coding regions and imply that molecular coevolution of LcrLFY and the L. crassa TFL1 ortholog, LcrTFL1, contributed to the evolution of rosette flowering.