Autonomous pathway
The autonomous pathway antagonizes FRIGIDA and functions in parallel with vernalization
Arabidopsis fca and fy mutants flower late in both long and short days. This lateness can be suppressed by either a vernalization treatment or by growth in low red/far red light conditions. These phenotypic properties are shared by a sub-set of other late-flowering mutants; namely ld, fld, fca, fpa, fve. These late-flowering recessive mutants have therefore been classified together with other flowering time mutants, in a genetically defined group known as the autonomous pathway. The level of FLC mRNA is increased in these mutants, indicating that the autonomous pathway normally functions to prevent FLC mRNA accumulation (Henderson et al 2005, Marquardt et al 2006).
FCA encodes an RNA binding protein with a WW protein interaction domain ( Macknight et al,1997). It interacts with FY, a conserved RNA processing factor.
Analysis of alternative processing of the FCA transcript demonstrates that FCA and FY can regulate polyadenylation sites in vivo (Simpson et al 2003, Quesada et al, 2003).
However, the lack of alternative FLC transcripts made it unclear whether they have the same mode of action on FLC. We used suppressor mutagenesis to identify components required for FCA/FY-mediated FLC repression. Our current model is that FCA and FY repress FLC via RNA processing/RNAi-mediated chromatin silencing.
A second RNAi-mediated chromatin silencing pathway directed at FLC has been found through the analysis of small RNAs homologous to FLC which map downstream of the major polyA site (Swiezewski et al 2007). These appear to mediate histone 3 K9 methylation in a very localised domain in the 3' region of FLC. So far our analysis suggests this chromatin silencing appears to act independently of FCA/FY activity.
Current areas of activity:
- Identification of additional genes required for FCA/FY down-regulation of FLC expression.
- Characterization of the RNA and protein partners of FCA.
