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MRNA destabilization by BTG1 and BTG2 maintains T cell quiescence

ABSTRACT: mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence

PROVIDER: PRJNA517898 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8503640_1.fastq.gz	Fastqsanger.gz
	SRR8503640_2.fastq.gz	Fastqsanger.gz
	SRR8503641_1.fastq.gz	Fastqsanger.gz
	SRR8503641_2.fastq.gz	Fastqsanger.gz
	SRR8503642_1.fastq.gz	Fastqsanger.gz

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mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [RNA-seq]

Project description:mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [RNA-seq]

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mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [mTAIL-seq]

Project description:mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [mTAIL-seq]

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mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [mTAIL-seq]

Project description:Quiescence is a cellular state in which cells undergo reversible cell cycle arrest in response to environmental challenges or lack of stimuli. When favourable conditions are engaged, the cells exit quiescence and start to proliferate. For example, quiescent stem cells and oocytes are activated by differentiation signals and fertilization, respectively. The regulation of quiescent state is also crucial for lymphocytes, such as T cells. Inappropriate activation of T cells often leads to autoimmune diseases and thus, the balance between quiescent and activated T cells must be preserved. Despite its importance, however, how T cells maintain the ‘quiescent state’ and exit from it remain largely unknown. Here, we identify BTG1 and BTG2 (BTG1/2) as factors responsible for T cell quiescence. Knockout of Btg1/2 in T cells resulted in a reduced threshold to T cell activation, increased proliferation and a concomitant reduction of the frequency of naive T cells. Loss of BTG1/2 rendered naive T cells to become spontaneously activated even without TCR stimuli. Interestingly, we found a global increase in mRNA abundance in naive T cells that lack BTG1/2. In addition, depletion of BTG1/2 led to an increase in mRNA half-life and poly(A) tail length. Thus, BTG1/2 promotes deadenylation and degradation of mRNA in naive T cells. Our study demonstrates a key mechanism underlying T cell quiescence, and suggests low mRNA abundance as a key feature for maintaining quiescent T cells.

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mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [RNA-seq]

Project description:Quiescence is a cellular state in which cells undergo reversible cell cycle arrest in response to environmental challenges or lack of stimuli. When favorable conditions are engaged, the cells exit quiescence and start to proliferate. For example, quiescent stem cells and oocytes are activated by differentiation signals and fertilization, respectively. The regulation of quiescent state is also crucial for lymphocytes, such as T cells. Inappropriate activation of T cells often leads to autoimmune diseases and thus, the balance between quiescent and activated T cells must be preserved. Despite its importance, however, how T cells maintain the ‘quiescent state’ and exit from it remain largely unknown. Here, we identify BTG1 and BTG2 (BTG1/2) as factors responsible for T cell quiescence. Knockout of Btg1/2 in T cells resulted in a reduced threshold to T cell activation, increased proliferation and a concomitant reduction of the frequency of naive T cells. Loss of BTG1/2 rendered naive T cells to become spontaneously activated even without TCR stimuli. Interestingly, we found a global increase in mRNA abundance in naive T cells that lack BTG1/2. In addition, depletion of BTG1/2 led to an increase in mRNA half-life and poly(A) tail length. Thus, BTG1/2 promotes deadenylation and degradation of mRNA in naive T cells. Our study demonstrates a key mechanism underlying T cell quiescence, and suggests low mRNA abundance as a key feature for maintaining quiescent T cells.

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BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

Project description:The human BTG1 and BTG2 genes are targeted by genetic alterations in hematological malignancies. In this study we examined the unique and overlapping functions of Btg1 and Btg2 in mouse B cell development. Mice deficient for Btg1 and Btg2 displayed the strongest phenotype with a decrease in B cell numbers in bone marrow due to impaired B cell commitment and immature B cell differentiation. To determine the underlying mechanism, microarray expression analyis was performed on early (B220+ CD43+) and late (B220+ CD43-) B cells of WT and Btg1;Btg2 dKO mice. Total RNA obtained from sorted B220+ CD43+ ( Hardy fractions ABC) and B220+ CD43- (Hardy fractions DEF) BM cells of WT and Btg1-/-;Btg2-/- mice. In total 4 samples were analyzed and no replicates were included.

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BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

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RNAseq of cultured neonatal rat ventricular cardiomyocytes treated with siRNA for Btg1 and Btg2 knockdown.

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