Zhang et al. BMC Genomics 2011, 12:63 http://www.biomedcentral.com/1471-2164/12/63 Page 15 of 20 Figure 8 Transcript level of six selected genes at different stages of spring shoot development in the mutant (black columns) and wild-type (grey columns). Stage 1: After self-pruning (undetermined lateral bud); Stage 2: Sepal primordia arise; Stage 3: Petal primordia arise; Stage 4: Stamen primordia arise; Stage 5: Pistil primordia arise; Stage 6: Fully developed floral bud. Relative transcript levels are calculated by real- time PCR with Actin as a standard. Data are means ± SE of three separate measurements. Exogenous GAs have been shown to inhibit flower bud formation not only in citrus [55] but also in apples [56], pears [57], and cherries and peaches [58]. This hormone is thus believed to strongly participate in regulating flower bud formation. Many GA biosynthetic and cata- bolism-related genes were also found in this study; how- ever, we did not find clear differences in the expression of GA biosynthetic and catabolism-related genes in the spring shoot apex samples of WT and MT genotypes before floral initiation occurred. So these data do not support the role of the GA pathway as the regulator of early flowering process in the MT, indicating that GA signal may be regulated during flowering development of the two gene types rather than only in the MT. In Arabidopsis, the floral induction signals from these four major flowering pathways (photoperiod, autono- mous, vernalization, and GA-induced pathways) are transmitted to three flowering pathway integrators, FT, SOC1, and LFY. When SOC1 is induced at the shoot apex, SOC1 together with AGL24 directly activates LFY. AP1, activated mainly by FT, is also necessary to estab- lish and maintain flower meristem identity [59]. When LFY and AP1 are established, flower development occurs at the anlagen of the shoot apical meristem according to the ABC model. During early flower development, AP1 activates the A function and represses three redundantly functioning flowering time genes, SOC1, AGL24, and SVP to prevent floral reversion. During late flower development, such repression is also necessary to acti- vate SEPALATA3 (SEP3) which is a coactivator of B and C function genes with LFY; otherwise SEP3 is sup- pressed by SOC1, AGL24, and SVP [59]. We have found citrus homologs for all of these genes except LFY and AGL24 in this study; one of the flowering-promoting genes was up-regulated in the MT library compared with the WT library (Table 3). Nevertheless, it is clear