pubmed: Genome Research https://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Search&db=PubMed&term=genome%20research%20%5Bjournal%5D NCBI: db=pubmed; Term=genome research [journal] en-us http://blogs.law.harvard.edu/tech/rss 1440 NCBI pubmed https://www.ncbi.nlm.nih.gov/entrez/query/static/gifs/iconsml.gif https://www.ncbi.nlm.nih.gov/sites/entrez PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites. Dehydration stress extends mRNA 3' untranslated regions with noncoding RNA functions in Arabidopsis. http://feedproxy.google.com/~r/genres/~3/oowR9AblbeE/28522613 Related Articles

Dehydration stress extends mRNA 3' untranslated regions with noncoding RNA functions in Arabidopsis.

Genome Res. 2017 May 18;:

Authors: Sun HX, Li Y, Niu QW, Chua NH

Abstract
The 3' untranslated regions (3' UTRs) of mRNAs play important roles in the regulation of mRNA localization, translation and stability. Alternative cleavage and polyadenylation (APA) generates mRNAs with different 3' UTRs, but the involvement of this process in stress response has not yet been clarified. Here, we report that a subset of stress-related genes exhibits 3' UTR extensions of their mRNAs during dehydration stress. These extended 3' UTRs have characteristics of long noncoding RNAs and likely do not interact with miRNAs. Functional studies using T-DNA insertion mutants reveal that they can act as antisense transcripts to repress expression levels of sense genes from the opposite strand, or can activate the transcription or lead to read-through transcription of their downstream genes. Further analysis suggests that transcripts with 3' UTR extensions have weaker poly(A) signals than those without 3' UTR extensions. Finally, we show that their biogenesis is partially dependent on a trans-acting factor FPA. Taken together, we report that dehydration stress could induce transcript 3' UTR extensions and elucidate a novel function for these stress-induced 3' UTR extensions as long noncoding RNAs in the regulation of their neighboring genes.

PMID: 28522613 [PubMed - as supplied by publisher]

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Sun HX, Li Y, Niu QW, Chua NH Genome Res PubMed:28522613 https://www.ncbi.nlm.nih.gov/pubmed/28522613?dopt=Abstract
GenomeVIP: a cloud platform for genomic variant discovery and interpretation. http://feedproxy.google.com/~r/genres/~3/jpq-aw2qQGg/28522612 Related Articles

GenomeVIP: a cloud platform for genomic variant discovery and interpretation.

Genome Res. 2017 May 18;:

Authors: Mashl RJ, Scott AD, Huang KL, Wyczalkowski MA, Yoon CJ, Niu B, DeNardo E, Yellapantula VD, Handsaker RE, Chen K, Koboldt DC, Ye K, Fenyƶ D, Raphael B, Wendl MC, Ding L

Abstract
Identifying genomic variants is a fundamental first step towards the understanding of the role of inherited and acquired variations in disease. The accelerating growth in the corpus of sequencing data that underpins such analysis is making the data-download bottleneck more evident, placing substantial burdens on the research community to keep pace. As a result, the search for alternative approaches to the traditional 'download and analyze' paradigm on local computing resources has led to a rapidly growing demand for cloud-computing solutions for genomics analysis. Here, we introduce the Genome Variant Investigation Platform (GenomeVIP), an open-source framework for performing genomics variant discovery and annotation using cloud- or local high-performance computing infrastructure. GenomeVIP orchestrates the analysis of whole genome and exome sequence data using a set of robust and popular task-specific tools, including VarScan, GATK, Pindel, BreakDancer, Strelka, and Genome STRiP, through a web interface. GenomeVIP has been employed for genomic analysis in large-data projects such as the TCGA PanCanAtlas and in other projects, such as the ICGC Pilots, CPTAC, ICGC-TCGA DREAM Challenges, and the 1000 Genomes SV Project. Here, we demonstrate GenomeVIP's ability to provide high-confidence annotated somatic, germline, and de novo variants of potential biological significance using publicly available datasets.

PMID: 28522612 [PubMed - as supplied by publisher]

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Mashl RJ, Scott AD, Huang KL, Wyczalkowski MA, Yoon CJ, Niu B, DeNardo E, Yellapantula VD, Handsaker RE, Chen K, Koboldt DC, Ye K, Fenyƶ D, Raphael B, Wendl MC, Ding L Genome Res PubMed:28522612 https://www.ncbi.nlm.nih.gov/pubmed/28522612?dopt=Abstract
Long terminal repeats power evolution of genes and gene expression programs in mammalian oocytes and zygotes. http://feedproxy.google.com/~r/genres/~3/ITTUYUUy8ls/28522611 Related Articles

Long terminal repeats power evolution of genes and gene expression programs in mammalian oocytes and zygotes.

Genome Res. 2017 May 18;:

Authors: Franke V, Ganesh S, Karlic R, Malik R, Pasulka J, Horvat F, Kuzman M, Fulka H, Cernohorska M, Urbanova J, Svobodova E, Ma J, Suzuki Y, Aoki F, Schultz RM, Vlahovicek K, Svoboda P

Abstract
Retrotransposons are 'copy-and-paste' insertional mutagens that substantially contribute to mammalian genome content. Retrotransposons often carry long terminal repeats (LTRs) for retrovirus-like reverse transcription and integration into the genome. We report an extraordinary impact of a group of LTRs from the mammalian endogenous retrovirus-related ERVL retrotransposon class on gene expression in the germline and beyond. In mouse, we identified >800 LTRs from ORR1, MT, MT2, and MLT families, which resemble mobile gene-remodeling platforms that supply promoters and first exons. The LTR-mediated gene remodeling also extends to hamster, human, and bovine oocytes. The LTRs function in a stage-specific manner during the oocyte-to-embryo transition by activating transcription, altering protein-coding sequences, producing non-coding RNAs, and even supporting evolution of new protein-coding genes. These functions result, for example, in recycling processed pseudogenes into mRNAs or lncRNAs with regulatory roles. The functional potential of the studied LTRs is even higher because we show that dormant LTR promoter activity can rescue loss of an essential upstream promoter. We also report a novel protein-coding gene evolution - D6Ertd527e, where an MT LTR provided a promoter and the 5' exon with a functional start codon while the bulk of the protein-coding sequence evolved through an CAG repeat expansion. Altogether, ERVL LTRs provide molecular mechanisms for stochastically scanning, rewiring, and recycling genetic information on an extraordinary scale. ERVL LTRs thus offer means for a comprehensive survey of genome's expression potential, tightly intertwining with gene expression and evolution in the germline.

PMID: 28522611 [PubMed - as supplied by publisher]

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Franke V, Ganesh S, Karlic R, Malik R, Pasulka J, Horvat F, Kuzman M, Fulka H, Cernohorska M, Urbanova J, Svobodova E, Ma J, Suzuki Y, Aoki F, Schultz RM, Vlahovicek K, Svoboda P Genome Res PubMed:28522611 https://www.ncbi.nlm.nih.gov/pubmed/28522611?dopt=Abstract