Flowering is a pivotal developmental process in response to the environment and determines the start of a new life cycle in plants. Woody plants usually possess a long juvenile nonflowering phase followed by an adult phase with repeated flowering cycles. The molecular mechanism underlying flowering regulation in woody plants is believed to be much more complex than that in annual herbs. In this review, we briefly describe the successive but distinct flowering processes in perennial trees, namely the vegetative phase change, the floral transition, floral organogenesis, and final blooming, and summarize in detail the most recent advances in understanding how woody plants regulate flowering through dynamic gene expression. Notably, the florigen gene FLOWERING LOCUS T(FT) and its antagonistic gene TERMINAL FLOWER 1 (TFL1) seem to play a central role in various flowering transition events. Flower development in different taxa requires interactions between floral homeotic genes together with AGL6 conferring floral organ identity. Finally, we illustrate the issues and corresponding measures of flowering regulation investigation. It is of great benefit to the future study of flowering in perennial trees.

Crape myrtle ( Lagerstroemia indica ) is a woody ornamental plant popularly grown because of its long-lasting, midsummer blooms and beautiful colors. The GL1 dominant mutant is the first chlorophyll-less mutant identified in crape myrtle. It was obtained from a natural yellow leaf bud mutation. We previously revealed that leaf color of the GL1 mutant is affected by light intensity. However, the mechanism of the GL1 mutant on light response remained unclear. The acclimation response of mutant and wild-type (WT) plants was assessed in a time series after transferring from low light (LL) to high light (HL) by analyzing chlorophyll synthesis precursor content, photosynthetic performance, and gene expression. In LL conditions, coproporphyrinogen III (Coprogen III) content had the greatest amount of accumulation in the mutant compared with WT, increasing by 100%. This suggested that the yellow leaf phenotype of the GL1 dominant mutant might be caused by disruption of coproporphyrinogen III oxidase (CPO) biosynthesis. Furthermore, the candidate gene, oxygen-independent CPO ( HEMN ), might only affect expression of upstream genes involved in chlorophyll metabolism in the mutant. Moreover, two genes, photosystem II (PSII) 10 kDa protein ( psbR ) and chlorophyll a/b binding protein gene ( CAB1 ), had decreased mRNA levels in the GL1 mutant within the first 96 h following LL/HL transfer compared with the WT. Hierarchical clustering revealed that these two genes shared a similar expression trend as the oxygen-dependent CPO ( HEMF) . These findings provide evidence that GL1 is highly coordinated with PSII stability and chloroplast biogenesis.