Unknown,Transcriptomics,Genomics,Proteomics

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Identification of dysregulated genes after deletion of miR-1-1 and miR-1-2


ABSTRACT: Purpose: The goals of this study are to identify dysregulated mRNAs in the heart after deletion of miR-1-1 and miR-1-2. Methods: Total RNAs were extracted from hearts at embryonic E15.5 (E15.5) or postnatal 2.5 days (P2.5) of miR-1s dHET and miR-1s dKO mice. mRNAs were purified using a poly-A selection approach and sequenced using Illumina HiSeq 2000. The sequence reads were aligned to the mouse reference genome (NCBI Build 37/mm9) using TopHat program (Bowtie algorithm). Transcript assembles and identification of differentially expressed genes were achieved using Cufflinks package. To account for expression bias due to transcript length, each sample transcript expression was normalized by using cufflinks algorithm with a FDR of 0.05. Results: Using 1.5-fold change as a cutoff, 997 and 653 transcripts were found to be upregulated and downregulated, respectively, in miR-1s dKO heart at P2.5. 423 transcripts were found to be upregulated and 653 were down-regulated in miR-1s dKO heart at E15.5. Many upregulated genes are directly involved in a fetal gene program. Conclusions: miR-1 directly represses a fetal gene program. We performed RNA deep-seq using postnatal 2.5 days (P2.5) heart from miR-1-1 and miR-1-2 double knockout mice and compared it to that of littermate control.

ORGANISM(S): Mus musculus

SUBMITTER: Yong Zhao 

PROVIDER: E-GEOD-45760 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Multifaceted roles of miR-1s in repressing the fetal gene program in the heart.

Wei Yusheng Y   Peng Siwu S   Wu Meng M   Sachidanandam Ravi R   Tu Zhidong Z   Zhang Shihong S   Falce Christine C   Sobie Eric A EA   Lebeche Djamel D   Zhao Yong Y  

Cell research 20140131 3


miRNAs are an important class of regulators that play roles in cellular homeostasis and disease. Muscle-specific miRNAs, miR-1-1 and miR-1-2, have been found to play important roles in regulating cell proliferation and cardiac function. Redundancy between miR-1-1 and miR-1-2 has previously impeded a full understanding of their roles in vivo. To determine how miR-1s regulate cardiac function in vivo, we generated mice lacking miR-1-1 and miR-1-2 without affecting nearby genes. miR-1 double knocko  ...[more]

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