In the warm growing season on the East Coast, broccoli crown development is often disrupted because insufficient cold accumulation for flower bud initiation and enlargement. As part of an effort to breed for adaptation to higher growing temperatures, we investigated whether the sensitivity is due to expression of one or more of the central genes involved in flower initiation. Broccoli transitions from vegetative to reproductive phase normally, it is the transition from reproductive meristem to floral meristem and flower bud that is arrested or delayed in warm temperatures. We compared the heat response of a highly sensitive genotype, ‘Clara’ and the most resistant available genotype ‘P13xP19’ (P. Griffiths, Cornell). Plants that had just entered the reproductive phase were exposed to temperatures that were either permissive (16/12°C Day/Night) or restrictive (28/22°C Day/Night) for three days, then RNA was isolated from the meristem. The RNA was sequenced, transcripts were identified and relative abundance of each transcript was determined. Transcripts were available corresponding to the genes of interest. The model is that various developmental and environmental cues affect expression of the integrator gene SOC. The expression level of SOC then influences a gene that maintains meristem (TFL1) and one that promotes flower development (LFY). The interplay between those genes in time and space is believed to control how big the meristem will get and when the meristem will start to make flowers. When LFY expression dominates, it promotes expression of AP1 (and paralogs) inducing floral primordia. A gene responsible for the heat sensitivity would have differential expression in heat only in the sensitive genotype. That was the case for TFL1 and one copy of SOC1, but not for the other genes. Therefore, heat sensitivity is caused by genes associated with meristem transition, not with the classic flower-initiation genes.
