In Arabidopsis, the transition to flowering is determined by the interaction between the plant competence for internal development and the environmental signs which favour the reproduction success. Nevertheless, plants exposed to environmental stress could accelerate their flowering. Some stress factors able to alter the flowering time, such as pathogen infection, extreme temperatures or high radiations, drive in an increase of some metabolites like etilene, abscisic acid and salicylic acid (SA) (Blee, 2002; Dempsey et al., 1999; Ni et al., 1996; Pastori y Foyer, 2002; Raskin, 1992). 
       Recent studies suggest that SA could be a regulator of the transition to flowering in Arabidopsis thaliana plants under stress conditions (Martínez et al., 2004). The accelerated flowering upon UV-C radiation required the synthesis as well as the accumulation of SA, since it will not occur in transgenic nahG plants that do not accumulate SA due to its rapid degradation to catechol. The way SA regulates the flowering time is up to date almost unknown.
       By using transgenic plants with the promoter of BGL2 gene (PR gene induced by SA) is fused to the reportert GUS gene, it was determined the time and space that correlate changes in internal levels of SA with the activation of gene expression leading to the transition to flowering. An increase in the GUS expression levels associated to the vascular tissue takes places the tenth day after sawing. Concomitantly, the expression of ICS1/SID2 gene, which codes for the isochorismate synthase 1 that synthesize SA in Arabidopsis (Wildermuth et al., 2001), and the FT gene, whose protein has been recently  characterized as a signal activating the flowering transition  (Jaeger y Wigge, 2007; Lin et al., 2007; Mathieu et al., 2007; Corbesier et al., 2007) was up-regulated. 
       The comparative analysis of the transcriptomes of SA-deficient plants (with late flowering phenotype) versus wild plants performed during the temporal frame previously described yielded 15 differentially expressed genes. We chose Pathogen and Circadian Controlled 1 (PCC1) since it was the only one responsive to UV-C light up-regulating its expression in wild plants but not in nahG plants. Besides, PCC1 was previously described as responsive to pathogen attacks, event characterized by the synthesis of SA, and also showing basal expression regulated by circadian clock (Sauerbrunn y Schlaich, 2004). PCC1 is thus a potential candidate to mediate between SA and its function as flowering time regulator. Moreover, the expression of PCC1 in long-day grown plants under no stress depends on the development stage of the plant, which gives support to a function as a regulator of other transitions of developmental phases. 
       The data obtained in the present work show that the expression of PCC1 is regulated by the circadian clock and is strictly dependent on the synthesis, accumulation and signalling of SA. Its activation requires the function of the photoperiod-dependent flowering time gene CO. SA-defficient plants showed constitutive overexpression of the clock component CCA1 and the loss of circadian regulation of CO thus explaining the unability to activate PCC1 gene expression. These data suggest that SA could have a role as a regulator of the circadian clock, output pathways or both of them.
       Transgenic plant with loss or gain of PCC1 function in different Arabidopsis genetic background allowed to demostrate that PCC1 regulates the timing of flowering. The reduced or increased expression of PCC1 in wild type and fve-3 mutant genetic background caused delayed or early flowering phenotype, respectively. However, in the mutant co-1 background the flowering timing is independent on the PCC1 transcript level, suggesting that stress-activated transition to flowering required not only PCC1 but also CO. The delay in flowering time observed in lines with reduced PCC1 expression in wild-type background correlated with lower expression of the FT integrator gene. By contrast, levels of SOC1 remained constant. These data suggest that PCC1 will interact with the photoperiod way in a point between CO and FT. Futhermore, the long day-grown PCC1 overexpression plants in Col-0 background looks like the wild type plants but the RNAi lines has a phenotype similar to the ft-4 mutant. They showed a more compact rosette with larger leaves and flowers and thicker stalks.
       The overexpression and RNAi transgenic lines in the Col-0, co-1 and fve-3 genetic backgrounds were tested for other process requiring SA synthesis such as defense against biothrophic pathogens (Malamy et al., 1990; Métraux et al., 1990; Reymond y Farmer, 1998) or senescence (Morris et al., 2000). Our data point out that PCC1 could have an antisenescing function, since the RNAi lines in wild-type background showed symptoms of darkness-induced sencescence earlier to that observed in non-transformed wild-type Col-0 control plants. However, no changes were observed between Col-0 and transgenic lines regarding resistance against Pseudomonas syringae.