Detailed gene information

Genes [306]

DCL1LHYGA2ox6MRG2CRY2ATPRMT10ATX2STOESD7, TIL1, ABO4NF-YC9, HAP5CPHYACIB4OTS2LWD1, ATAN11UBC1GAI, RGA2GA3OX1TPLCSTF77ARP4AFR2GIPFT1, MED25TEM1, EDF1CIB5CUL3AVOZ1GA2ox2SUF4FRL2RCD1FBH1GA2ox4CPK33GA2ox7FBH3, AKS1, BHLH122ASH2R, TROHTA9SPA4SPL4RRP6L1NF-YC3HUB2MED13, GCT, MAB2VIM1, ORTH2OTS1, ULP1DVIP5LDL1FTVIM2RGL1AT-STUbl4FKF1, ADO3TEM2, RAV2AP1CDF5CSTF64PHLAFR1SDG26, ASHH1FLM, MAF1, AGL27EFS, SDG8GA2ox1TPS1APL, WDY, FEGA2, ATKS1ELF7PRP8, SUS2, EMB33GA3OX2RGA1UBC2EFMELF8, VIP6ABH1, CBP80CPK6FDP, BZIP27PHYBVIL3, VEL2LKP2MIR156GFVE, MSI4GLK1, GPRI1FIO1GRP7, CCR2MED18SVPAGL17CLF, SDG1SUVR5MIR156AELF3ATCMIR172ATOE1, RAP2.7PUB12FLXUGT87A2ATX1, SDG27COP1SPL3FES1CDF4GA2ox3NF-YA4JMJ15, MEE27SRO1AS1HTA8NF-YB1, HAP3ASNZESD6, HOS1ELF4SPL9FBH4, AKS3VOZ2PIF4FPASDG7, ASSH3CKB4HUB1AHL22AGL6SOC1, AGL20BRM, CHR2LRB1SPA1PRR9CCA1RFI2HULK2AKIN10, SNRK1.1MBD9GASA5RGL2MYR2FLKGID1ACOL9FLD, RSI1MIR172CUBP13PIE1LDL2SPL5SPA3BRC1, TCP18VRN1DNFFIE1, FIS3JMJ30TICPHP, CDC73AtBMI1CVIL1, VRN5LWD2ICE1, SCRMSSRP1, HMG, NFDMYB30ARP6, SUF3, ESD1SUS4DCL3ATJ3HDA9JMJ32, JMJD5PUB13LUX, PCL1CDF3REF6, JMJ12UBP26WDR5ALNK2HTA11SMZAGL16INO80AGL18SPL15PIF5, PIL6CKB3LRB2, POB1GID1BHULK3MED12, CCT, CRPFRILIF2LDGA1AtNDXMED16, SFR6CRY1FBH2DET1, FUS2SPT16XAL2, AGL14NF-YB3, HAP3CESD4PHYDFCAVRN2PHYETSFJMJ14, PKDM7B, JMJ4GA2ox8EBSAGL19CAD2, RML1, GSH1AGL24PGI1MOS1GA20ox1FWA, HDG6WRKY34, MSP3ULT1HXK1, GIN2VIP3, SKI8VIL2, VEL1MIR156BSKB1, PRMT5MIR156CATH1CIB1FDAP2MRG1CSP2, GRP2BBX19SHL1, SHLHB16, ATHB16PRR7TFL1ELF6MIR172BSUC9UBP12FTIP1GA20OX3HAM2, HAG5, HAC11FLC, AGL25, FLFMIR156DEMF1MIR156ENF-YA1, HAP2BFYAGL15BAF60, CHC1COFRL1, SUF8RGL3TFL2, LHP1MYR1DCL4HUA2RUP2, EFO2PRR5FPF1MIR156FGID1CPHYCRRP6L2SEF, SWC6RVE2, CIR1VIM3, ORTH1CDF2HLP1ATXR7, SDG25IDD8, NUCGLK2CBP20YAF9A, TAF14B, GAS41CUL4NF-YB2, HAP3BADG1, APS1CIB2LATEPRMT4AEMF2, CYR1GA20ox2PGM1MIR156HZTLVIN3COL5MSI1SRR1PRR3TOE2SIZ1FUL, AGL8HDA5VIP4TOC1LFYFLX4, FLL4BFTCDF1HDA6, RTS1NF-YC4GIS5, EMB2780LNK1HAM1CDKC;2MAF2, AGL31MAF3, AGL70MAF4, AGL69MAF5, AGL68TOE3

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Publications

Lee I et al., 1993, Mol. Gen. Genet.
Clarke J H et al., 1994, Mol. Gen. Genet.
Lee I et al., 1995, Plant Physiol.
Johanson U et al., 2000, Science
Michaels S D et al., 2004, Proc. Natl. Acad. Sci. U.S.A.
Stinchcombe J R et al., 2004, Proc. Natl. Acad. Sci. U.S.A.
Choi K et al., 2011, Plant Cell
Lee J et al., 2013, Nat Commun

Appears in the following schemes

FLC regulation through protein complexes
FLC regulation during a cold period

Protein function

Encodes a transcription factor that positively regulates the expression of FLC and is a major determinant regulating natural variation of Arabidopsis flowering time.

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Phenotype

Overexpressor:
Expression of a functional FRI allele in fri mutants leads to late flowering under both SD and LD conditions. [Michaels et al., 2004][Lee et al., 1995][Lee et al., 1995][Schmitz et al., 2005]

Remarks:
FRIGIDA is required for FLC expression in winter annual accessions. Many loss-of-function alleles have been described in early flowering summer annuals. [Clarke et al., 1994]

Remarks:
Introgression of a FRI allele from winter accessions into Col or Ler background leads to a very late flowering-time and increased vernalization-responsiveness. [Michaels et al., 2004][Lee et al., 1995]

Overexpressor:
The overexpression of FRI in a FRI-containing background does not further increase the late flowering-time phenotype. [Michaels et al., 2004][Lee et al., 1995][Lee et al., 1995][Schmitz et al., 2005]

Function:
Required for the regulation of flowering time in the late-flowering phenotype. Involved in the enrichment of a WDR5A-containing COMPASS-like complex at the FLOWERING LOCUS C that trimethylates histone H3 Lys-4 , leading to FLC up-regulation and RNA levels increase (PubMed:19567704). Variants with an early-flowering phenotype (Including cv. Columbia, cv. Landsberg Erecta and cv. Wassilewskija) show loss-of-function mutations of FRI. Able to delay flowering independently of FRL1 activity. Dispensable for the reactivation of FLC in early embryogenesis, but required to maintain high levels of FLC expression in later embryonic and vegetative development. Suppresses the repression of FLC by the autonomous pathway, but has no effect on the expression of the genes involved in this pathway. [Data from UniProt]

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Regulators, targets and interactors

Downstream actors

causality
FLC, AGL25, FLF -- [Johanson et al., 2000] -- [View TAIR record]

Upstream actors

causality
CUL3A -- [Hu et al., 2014] -- [View TAIR record]

LRB2, POB1 -- [Hu et al., 2014] -- [View TAIR record]

LRB1 -- [Hu et al., 2014] -- [View TAIR record]

Protein-protein interactions

CUL3A -- [Christians et al., 2012] -- [View TAIR record]

SUF4 -- [Choi et al., 2011] -- [View TAIR record]

FLX -- [Choi et al., 2011] -- [View TAIR record]

FES1 -- [Choi et al., 2011] -- [View TAIR record]

LRB1 -- [Christians et al., 2012] -- [View TAIR record]

LRB2, POB1 -- [Christians et al., 2012] -- [View TAIR record]

FRL1, SUF8 -- [Choi et al., 2011] -- [View TAIR record]

FRI interaction network

Downstream and upstream flowering-related genes

Physical interactions with other flowering-related proteins