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

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

PROVIDER: PRJNA517726 | 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

Project description:mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence

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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

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

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