Unknown,Transcriptomics,Genomics,Proteomics

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Pre-mRNA splicing factor atsf1-2 mutant seedlings

ABSTRACT: Analysis of atsf1-2 mutant seedlings for pre-mRNA splicing defect. The atsf1-2 mutant is a homozygous T-DNA insertion line isolated from a SALK line, SALK_062177. Results identify transcripts with altered alternative splicing pattern in the atsf1-2 mutant. We used microarrays to examine the transcriptome profile in the atsf1-2 mutant and identified genes of which transcript levels were changed significantly. Arabidopsis seedlings were grown for 9 days under long day condition. They were then used for RNA extraction and hybridization on Affymetrix ATH1 Genome Array. Three replicates for Col-0 (control) and atsf1-2 (mutant) were compared respectively.

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: Jeong-Kook Kim

PROVIDER: E-GEOD-48114 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Recent genetic studies in mice have established a key role for the nuclear receptor coregulator Trim24 in liver tumor suppression and provided evidence that Trim24 suppresses hepatocarcinogenesis by inhibiting retinoic acid receptor alpha (Rara)-dependent transcription and cell proliferation. However, it is unknown which downstream targets of Rara regulated by Trim24 are critical for tumorigenesis. We report here that loss of Trim24 results in the overexpression of interferon (IFN)/STAT pathway genes in the liver, a process that occurs early in tumorigenesis and is more pronounced in tumors, despite the enhanced expression, late in the disease, of negative regulators such as Usp18, Socs1 and Socs2. Remarkably, Rara haplodeficiency, which was previously shown to suppress tumor development in Trim24-/- mice, also suppresses overexpression of the IFN/STAT pathway, thus providing evidence for a cross-pathway control that may be relevant to the transformation process. Biochemical studies revealed that Trim24 binds to the retinoic acid (RA)-responsive element in the Stat1 promoter in a RA-dependent manner and represses RA-induced transcription from this promoter. Together, these results identify Trim24 as a novel regulator of the IFN/STAT pathway and indicate that Trim24-mediated repression of the IFN/STAT signaling through Rara inhibition may play a critical role in preventing liver cancer. Generation of Trim24-/- mice has been described previously (Khetchoumian et al., 2007) by gene disruption. To generate compound mutant mice with a single allele of Rara deleted in the Trim24 -/- mutant background, we crossed Trim24 -/- mice with Rara+/- mice. The resulting Trim24+/- Rara+/- mice were generated in the hybrid (C57BL/6 (60%), 129/Sv (40%)) genetic background. These double heterozygous Trim24+/- Rara+/- mice were intercrossed to generate Trim24 -/-, Trim24 -/- Rara+/- and wild-type mice. Transcriptional profiling of mice at 5-weeks and 14-weeks of age.

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Pre-mRNA splicing factor atsf1-2 mutant seedlings

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