Bursty gene expression and mRNA decay pathways orchestrate B cell activation.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 34860551.
- Also identified by DOI 10.1126/sciadv.abm0819 and PMC identifier 8641932.
- Licence recorded as CC BY-NC.
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Abstract
It is well established that the helix-loop-helix proteins, E2A and E2-2, promote B cell activation. Here, we examined how during the course of B cell activation <i>E2A</i> and <i>E2-2</i> gene expression is regulated. We found that <i>E2A</i> and <i>E2-2</i> mRNA abundance concomitantly increased in activated B cells. The increase in <i>E2A</i> and <i>E2-2</i> mRNA abundance correlated with increased cell growth. Elevated <i>E2A</i> and <i>E2-2</i> mRNA abundance was instructed by increased transcriptional bursting frequencies and elevated <i>E2A</i> and <i>E2-2</i> mRNA half-lives. The increase in <i>E2A</i> and <i>E2-2</i> bursting frequencies often occurred at shared interchromosomal transcriptional hubs. We suggest that in naïve B cells low <i>E2A</i> and <i>E2-2</i> bursting frequencies and high <i>E2A</i> and <i>E2-2</i> mRNA decay rates instruct noisy gene expression that allows a clonal and swift response to invading pathogens whereas in activated B cells increased transcriptional bursting and low mRNA decay rates dictate an activated B lineage gene program.