Claim · model-written summary
AtRRP6L mutants show little or no ASL transcript.
- Taxon
- Arabidopsis
Arabidopsise0 - Treatment
- these mutantse2
- Outcome
- ASL transcripte2
- Direction
- little or noe2
Not reportedMaterialGeneCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleComparatorSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“mutations of two Arabidopsis genes encoding nuclear exosome components AtRRP6L1 and AtRRP6L2, cause de-repression of the main flowering repressor FLOWERING LOCUS C (FLC)”
e2“The AtRRP6L proteins function as the main regulators of ASL synthesis, as these mutants show little or no ASL transcript”
Title
Jun-Hye Shin; Julia A. Chekanova PLoS Genetics 2014. doi:10.1371/journal.pgen.1004612
Other claims from this paper (14)
- Intervention effect Mutations of AtRRP6L1 and AtRRP6L2 de-repress the flowering repressor FLC.
- Intervention effect Mutations of AtRRP6L1 and AtRRP6L2 delay flowering in early-flowering Arabidopsis ecotypes.
- Intervention effect AtRRP6L mutations affect the expression of the FLC regulatory antisense RNAs AS I and II.
- Intervention effect AtRRP6L mutations increase H3K4 trimethylation (H3K4me3) at FLC.
- Mechanism AtRRP6L1 and AtRRP6L2 function redundantly in the regulation of FLC.
- Mechanism AtRRP6L1 and AtRRP6L2 regulate FLC independently of the exosome core complex.
- Observation A novel long non-coding, non-polyadenylated antisense transcript (ASL) originates from the FLC locus in wild type Arabidopsis plants.
- Mechanism AtRRP6L proteins are the main regulators of ASL synthesis.
- Association Unlike ASI/II, ASL associates with H3K27me3 regions of FLC.
- Mechanism ASL may function in the maintenance of H3K27 trimethylation during vegetative growth.
- Intervention effect AtRRP6L mutations affect H3K27me3 levels and nucleosome density at the FLC locus.
- Observation AtRRP6L1 physically associates with the ASL transcript and directly interacts with the FLC locus.
- Mechanism AtRRP6L proteins may maintain H3K27me3 at FLC via regulating ASL.
- Mechanism AtRRP6L proteins may participate in multiple FLC silencing pathways by regulating diverse antisense RNAs.