No abstract

Chimeric genes contribute to the evolution of diverse functions in plants and animals. However, new chimeric genes also increase the risk of developmental defects. Here, we show that the chimeric gene ( ) is responsible for genic male sterility in the widely used canola line 7365A ( ). originated via exon shuffling ∼4.6 million years ago. It causes defects in the normal functions of plastids and induces aborted anther formation and/or albino leaves and buds. Evidence of the age of the mutation, its tissue expression pattern, and its sublocalization indicated that it coevolved with (). In , results in complete male sterility that can be rescued by , suggesting that might restore fertility through effects on protein level. Another suppressor gene, , rescues sterility by reducing the level of transcription of Our results suggest that plants have coevolved altered transcription patterns and neofunctionalization of duplicated genes that can block developmental defects resulting from detrimental chimeric genes.

The appropriate timing of flowering is critical for plant reproductive success. Although the FLOWERING LOCUS T (FT)-FD module plays crucial roles in the photoperiodic flowering pathway, the underlying mechanisms and signaling pathways involved still remain elusive. Here, we demonstrate that class II TCP transcription factors (TFs) integrate into the FT-FD complex to control floral initiation in Arabidopsis (Arabidopsis thaliana). Class II CINCINNATA (CIN) TCP TFs function as transcriptional activators by directly binding to the promoters of downstream floral meristem identity genes, such as APETALA1 (AP1). In addition, these TCPs directly interact with FD, a basic Leu zipper TF that plays a critical role in photoperiodic flowering, which further activates AP1 expression. Genetic analyses indicated that class II CIN TCP TFs function synergistically with FT and FD, to positively regulate flowering in an AP1-dependent manner. Thus, our results provide compelling evidence that class II CIN TCP TFs act directly at the AP1 promoter to enhance its transcription, thus further elucidating the molecular mechanisms underlying the regulation of photoperiodic flowering in Arabidopsis.