High impact information on FRI

• Two functionally distinct PHYC haplotype groups are distributed in a latitudinal cline dependent on FRIGIDA, a locus that together with FLOWERING LOCUS C explains a large portion of the variation in A. thaliana flowering time [1].
• Most of the early-flowering ecotypes analyzed carry FRI alleles containing one of two different deletions that disrupt the open reading frame [2].
• A MADS-domain gene, AGAMOUS-LIKE 20 (AGL20), was identified as a dominant FRI suppressor in activation tagging mutagenesis [3].
• SUF4 protein interacts with FRI and FRIGIDA-LIKE1 (FRL1), two genes for which single mutations have the same phenotype as suf4 [4].
• Thus, we propose that LD binds to SUF4 to suppress its activity in the absence of FRI [4].

Biological context of FRI

• We have identified a locus, FRIGIDA-ESSENTIAL 1 (FES1), which, like FRI, is specifically required for the upregulation of FLC expression [5].
• FES1 is predicted to encode a protein with a CCCH zinc finger, but the predicted sequence does not otherwise share significant similarity with other known proteins. fes1 is a complete suppressor of FRI-mediated delayed flowering, but has little effect on the late-flowering phenotype of autonomous-pathway mutants [5].
• The maintenance and propagation of 20 independent nonfunctional FRI haplotypes suggest that the loss-of-function mutations can confer a strong selective advantage [6].
• In addition, we have found that the downregulation of SUPPRESSOR OF OVEREXPRESSION OF CONSTANS1 by FRI and autonomous pathway mutants also is mediated by FLC [7].
• There is significant linkage disequilibrium between FRI and FLC despite their location on separate chromosomes [8].

Regulatory relationships of FRI

• Lesions in the mRNA cap-binding gene ABA HYPERSENSITIVE 1 suppress FRIGIDA-mediated delayed flowering in Arabidopsis [9].
• FRI upregulates FLC expression that represses flowering in Arabidopsis [10].
• Our data suggest that FRI up-regulates FLC expression through a cotranscriptional mechanism involving direct physical interaction with the nuclear CBC with concomitant effects on FLC transcription and splicing [11].

Other interactions of FRI

• The expression of FLC is increased by FRIGIDA (FRI) but decreased by vernalization, a long period of cold exposure that accelerates flowering [4].
• The suppression of late flowering is caused by the inability of FRI to increase FLC mRNA levels in the abh1 mutant background [9].
• Overexpression of AGL20 suppresses not only the late flowering of plants that have functional FRI and FLC alleles but also the delayed phase transitions during the vegetative stages of plant development [3].
• Mutations in PHOTOPERIOD-INDEPENDENT EARLY FLOWERING1 (PIE1) suppress the FLC-mediated delay of flowering as a result of the presence of FRIGIDA or of mutations in autonomous pathway genes [12].
• The suf3 mutation caused a decrease in the transcript level of FLC in both a FRI-containing line and autonomous pathway mutants [13].

Analytical, diagnostic and therapeutic context of FRI

• Sequence analysis of FRI revealed which accessions were likely to carry functional alleles, and, from comparison of flowering time with allelic type, we estimate that approximately 70% of flowering time variation can be accounted for by allelic variation of FRI [6].

References