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Sirena1: The most abundant lncRNA in mouse oocytes brings together post-transcriptional regulations and mitochondrial distribution (mouse dev_stages)

ABSTRACT: Sirena1: The most abundant lncRNA in mouse oocytes brings together post-transcriptional regulations and mitochondrial distribution (mouse dev_stages)

PROVIDER: PRJNA565671 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10123258.fastq.gz	Fastqsanger.gz
	SRR10123259.fastq.gz	Fastqsanger.gz
	SRR10123260.fastq.gz	Fastqsanger.gz
	SRR10123261.fastq.gz	Fastqsanger.gz
	SRR10123262.fastq.gz	Fastqsanger.gz

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Sirena1: The most abundant lncRNA in mouse oocytes brings together post-transcriptional regulations and mitochondrial distribution

Project description:Sirena1: The most abundant lncRNA in mouse oocytes brings together post-transcriptional regulations and mitochondrial distribution

| PRJNA565935 | ENA

Sirena1: The most abundant lncRNA in mouse oocytes brings together post-transcriptional regulations and mitochondrial distribution (rat wild-type GV oocytes)

Project description:Sirena1: The most abundant lncRNA in mouse oocytes brings together post-transcriptional regulations and mitochondrial distribution (rat wild-type GV oocytes)

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Sirena1: The most abundant lncRNA in mouse oocytes brings together post-transcriptional regulations and mitochondrial distribution (mouse dev_stages)

Project description:Long non-coding RNAs (lncRNAs) are a large group of rapidly evolving non-coding RNAs. Tens of thousands of lncRNAs were identified but function has been assigned to relatively few. LncRNAs expressed in mouse oocytes have been annotated but their contribution to oocyte development and early development remains unknown. Here, we report evolutionary history and functional analysis of Sirena1, maternal lncRNA that is the most expressed maternal lncRNA and 10th most abundant Pol II transcript in mouse oocytes.

2019-09-30 | GSE137458 | GEO

Sirena1: The most abundant lncRNA in mouse oocytes brings together post-transcriptional regulations and mitochondrial distribution (rat wild-type GV oocytes)

2019-09-30 | GSE137562 | GEO

Sirena1: The most abundant lncRNA in mouse oocytes brings together post-transcriptional regulations and mitochondrial distribution

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-09-30 | GSE137563 | GEO

How Moving Together Brings Us Together: When Coordinated Rhythmic Movement Affects Cooperation.

Project description:Although it is well established that rhythmically coordinating with a social partner can increase cooperation, it is as yet unclear when and why intentional coordination has such effects. We distinguish three dimensions along which explanations might vary. First, pro-social effects might require in-phase synchrony or simply coordination. Second, the effects of rhythmic movements on cooperation might be direct or mediated by an intervening variable. Third, the pro-social effects might occur in proportion to the quality of the coordination, or occur once some threshold amount of coordination has occurred. We report an experiment and two follow-ups which sought to identify which classes of models are required to account for the positive effects of coordinated rhythmic movement on cooperation. Across the studies, we found evidence (1) that coordination, and not just synchrony, can have pro-social consequences (so long as the social nature of the task is perceived), (2) that the effects of intentional coordination are direct, not mediated, and (3) that the degree of the coordination did not predict the degree of cooperation. The fact of inter-personal coordination (moving together in time and in a social context) is all that's required for pro-social effects. We suggest that future research should use the kind of carefully controllable experimental task used here to continue to develop explanations for when and why coordination affects pro-social behaviors.

| S-EPMC5177969 | biostudies-literature

Activity-dependent gene regulations in PV+ interneurons

Project description:Activity-dependent gene regulations in PV+ interneurons

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BLOC-1 Brings Together the Actin and Microtubule Cytoskeletons to Generate Recycling Endosomes.

Project description:Recycling endosomes consist of a tubular network that emerges from vacuolar sorting endosomes and diverts cargoes toward the cell surface, the Golgi, or lysosome-related organelles. How recycling tubules are formed remains unknown. We show that recycling endosome biogenesis requires the protein complex BLOC-1. Mutations in BLOC-1 subunits underlie an inherited disorder characterized by albinism, the Hermansky-Pudlak Syndrome, and are associated with schizophrenia risk. We show here that BLOC-1 coordinates the kinesin KIF13A-dependent pulling of endosomal tubules along microtubules to the Annexin A2/actin-dependent stabilization and detachment of recycling tubules. These components cooperate to extend, stabilize and form tubular endosomal carriers that function in cargo recycling and in the biogenesis of pigment granules in melanocytic cells. By shaping recycling endosomal tubules, our data reveal that dysfunction of the BLOC-1-KIF13A-Annexin A2 molecular network underlies the pathophysiology of neurological and pigmentary disorders.

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The C-Ala domain brings together editing and aminoacylation functions on one tRNA.

Project description:Protein synthesis involves the accurate attachment of amino acids to their matching transfer RNA (tRNA) molecules. Mistranslating the amino acids serine or glycine for alanine is prevented by the function of independent but collaborative aminoacylation and editing domains of alanyl-tRNA synthetases (AlaRSs). We show that the C-Ala domain plays a key role in AlaRS function. The C-Ala domain is universally tethered to the editing domain both in AlaRS and in many homologous free-standing editing proteins. Crystal structure and functional analyses showed that C-Ala forms an ancient single-stranded nucleic acid binding motif that promotes cooperative binding of both aminoacylation and editing domains to tRNA(Ala). In addition, C-Ala may have played an essential role in the evolution of AlaRSs by coupling aminoacylation to editing to prevent mistranslation.

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