Information report for Pta011107
Gene Details
Functional Annotation
- TrEMBL: A0A1L7U5Z3 — A0A1L7U5Z3_FUSMA; Uncharacterized protein
- TrEMBL: A0A1L7W4M0 — A0A1L7W4M0_FUSPR; Uncharacterized protein
- TrEMBL: A0A2H3GN48 — A0A2H3GN48_FUSOX; Uncharacterized protein
- TrEMBL: A0A2H3SDV5 — A0A2H3SDV5_GIBFU; Uncharacterized protein
- TrEMBL: A0A2H3TPP3 — A0A2H3TPP3_FUSOX; Uncharacterized protein
- TrEMBL: A0A2K0WMN1 — A0A2K0WMN1_GIBNY; Uncharacterized protein
- TrEMBL: A0A3L6N7C9 — A0A3L6N7C9_FUSOX; Uncharacterized protein
- TrEMBL: F9F398 — F9F398_FUSOF; Uncharacterized protein
- TrEMBL: N1RJS1 — N1RJS1_FUSC4; Uncharacterized protein
- TrEMBL: N4UV10 — N4UV10_FUSC1; Uncharacterized protein
- TrEMBL: S0EID7 — S0EID7_GIBF5; Uncharacterized protein
- TrEMBL: W7N3F5 — W7N3F5_GIBM7; Uncharacterized protein
- TrEMBL: W9HW66 — W9HW66_9HYPO; Uncharacterized protein
- TrEMBL: W9JUH6 — W9JUH6_FUSOX; Uncharacterized protein
- TrEMBL: W9NYA2 — W9NYA2_FUSOX; Uncharacterized protein
- TrEMBL: W9ZNL5 — W9ZNL5_FUSOX; Uncharacterized protein
- TrEMBL: X0C798 — X0C798_FUSOX; Uncharacterized protein
- TrEMBL: X0ICC1 — X0ICC1_FUSOX; Uncharacterized protein
- TrEMBL: X0KA99 — X0KA99_FUSOX; Uncharacterized protein
- TrEMBL: X0LMU4 — X0LMU4_FUSOX; Uncharacterized protein
- STRING: FVEG_10334T0 — (Fusarium verticillioides)
- STRING: CCT73602 — (Fusarium fujikuroi)
- STRING: FOXG_11487P0 — (Fusarium oxysporum)
Family Introduction
- We show that Arabidopsis FHY3 and FAR1, which encode two proteins related to Mutator-like transposases, act together to modulate phyA signaling by directly activating the transcription of FHY1 and FHL, whose products are essential for light-induced phyA nuclear accumulation and subsequent light responses. FHY3 and FAR1 have separable DNA binding and transcriptional activation domains that are highly conserved in Mutator-like transposases. Further, expression of FHY3 and FAR1 is negatively regulated by phyA signaling. We propose that FHY3 and FAR1 represent transcription factors that have been co-opted from an ancient Mutator-like transposase(s) to modulate phyA-signaling homeostasis in higher plants.
- We next used a yeast one-hybrid assay to delineate the DNA sequences to which FHY3 and FAR1 bind. GAD-FHY3 or GAD-FAR1 fusion proteins (GAD, GAL4 transcriptional activation domain), but not GAD alone, activated the LacZ reporter genes driven by the FHY1 and FHL promoters. Deletion analysis narrowed down the FHY3/FAR1 binding site to a 39-bp promoter subfragment located on the ‘a’ fragment for both FHY1 and FHL. Notably, these subfragments share a stretch of consensus sequence, 5’-TTCACGCGCC-3’. Mutating the core sequence ‘CACGCGC’ of this motif (m2 and m3 for FHY1, m5 for FHL) abolished the reporter gene activation by both GAD-FHY3 and GAD-FAR1. Mutating the flanking sequences (m1 and m4) did not obviously affect the reporter gene activation by GAD-FAR1, but clearly reduced activation by GAD-FHY3. Thus, ‘CACGCGC’ likely defines a cis-element that confers specific binding for FHY3 and FAR1 and is named FBS for FHY3-FAR1 binding site.
Literature and News
Sequences
CDS Sequence:
- >Pta011107|Pinus_taeda|FAR1|PUT-157a-Pinus_taeda-24590
ATGCCGAATATACCACCTCCAGCGCTATTACCCCCACCAGAAGGTATATTTAGGACCTTCGAAGATTTGATGGCTTCCGTCCAGCGCGTTGCAAAGGACCAGGGATACGGAATTGTCAAGCTGCGCGCCTCAAACTACCGCGACGGAAAACCCACCCGTTATGATCTCGTTTGCGACCGCGGTGGTGTCAAGTACAACAGCACTGCCAAGAAGCGCAACCCTTCGACGCGCAAAATTGATTGTCCCTTCCGCGCCAAGGCTGTTTGTGAAGTTCAGCTCGGAAACCAGTGGCGTTTTGCTATCCAAGAGGGACGTCACAACCACGAGCCACGAGCTCCCTCTGGCACGCCTGGTCAGGAGAACGCGCCGCTGGCTACATCGATCCGATCCTTCACTAATAAACTCGACCGCCTGAACCACGACATGGCCCAGGGTCTAATGCGCATTGAGCAGCGTCTCGATAACATCGAGAAGCGCATGGACAGTCTTGAAGCCCGAGCTGGAGGCGGCTACGAACCACGCTTCCAGGCTATTGAACAAAGACTCCAGGGGATGGAAGGTCCTCGCATGGATGGGATGGGTATGGACGATGTCGAAACACGTCTTCTAGCCTCGACGGTAATGTAG
Protein Sequence:
- >Pta011107|Pinus_taeda|FAR1|PUT-157a-Pinus_taeda-24590
MPNIPPPALLPPPEGIFRTFEDLMASVQRVAKDQGYGIVKLRASNYRDGKPTRYDLVCDRGGVKYNSTAKKRNPSTRKIDCPFRAKAVCEVQLGNQWRFAIQEGRHNHEPRAPSGTPGQENAPLATSIRSFTNKLDRLNHDMAQGLMRIEQRLDNIEKRMDSLEARAGGGYEPRFQAIEQRLQGMEGPRMDGMGMDDVETRLLASTVM