Year-end Sale % OFF 
Abstract
Differences in the timing of vegetative-to-reproductive phase transition have evolved independently and repeatedly in different plant species. Due to their specific biological functions and positions in pathways, some genes are important targets of repeated evolution – independent mutations on these genes caused the evolution of similar phenotypes in distantly related organisms. While many studies have investigated these genes, it remains unclear how gene duplications influence repeated phenotypic evolution. Here we characterized the genetic architecture underlying a novel rapid-flowering phenotype in Boechera stricta and investigated the candidate genes BsFLC1 and BsFLC2. The expression patterns of BsFLC1 suggested its function in flowering time suppression, and the deletion of BsFLC1 is associated with rapid flowering and loss of vernalization requirement. In contrast, BsFLC2 did not appear to be associated with flowering and had accumulated multiple amino acid substitutions in the relatively short evolutionary timeframe after gene duplication. These non-synonymous substitutions greatly changed the physicochemical properties of the original amino acids, concentrated non-randomly near a protein-interacting domain, and had greater substitution rate than synonymous changes. Here we suggested that, after recent gene duplication of the FLC gene, the evolution of rapid phenology was made possible by the change of BsFLC2 expression pattern or protein sequences and the deletion of BsFLC1.
Highlights
Disentangling the genetic architecture underlying evolutionary changes is a critical task for evolutionary geneticists, and the evolution of parallel phenotypic changes is intriguing
Since the flowering of MR24 was not affected by vernalization, we investigated homologs for the candidate genes FLOWERING LOCUS C (FLC) in the rapid-flowering MR24 and slow-flowering MR7A accessions
Previous work identified two FLC copies in Boechera (Schranz et al, 2007), and these two copies showed distinct patterns between MR24 and MR7A (Figure 2): while BsFLC2 is present and expressed in both accessions, the BsFLC1 locus was only amplified in the slow-flowering MR7A but not the rapidflowering MR24 accession
Summary
Disentangling the genetic architecture underlying evolutionary changes is a critical task for evolutionary geneticists, and the evolution of parallel phenotypic changes is intriguing. Independent loss-of-function events, on the other hand, can happen in many ways, such as point mutation creating a premature stop codon, large insertions disrupting a gene, deletions removing the whole gene or important functional sites, or gene disruption by structural rearrangements. One mutation in the original copy can cause loss of function if the duplicated copy does not retain the original function This can happen if (1) only a portion of the gene was duplicated, creating a truncated and non-functional new copy, (2) the duplication event did not cover important regulatory regions flanking the gene, making the new copy cease to express in the same tissue or time, or (3) the new copy was intact and had the same spatiotemporal patterns of expression but later underwent amino acid substitutions changing the protein function. Note that while possibility (1) and (2) indicate a genetic change caused by the duplication event itself, possibility (3) focuses on changes after the duplication
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
