IgM RNA switch from membrane to secretory form is prevented by adding antireceptor antibody to bacterial lipopolysaccharide-stimulated murine primary B-cell cultures.

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Abstract
Bacterial lipopolysaccharide (LPS) induces proliferation of resting primary murine B lymphocytes and their differentiation into Ig-secreting cells. This is accompanied by an increase in the rate of Ig gene transcription and the accumulation of .mu. heavy chain secretory mRNA. Specific antiantigen receptor antibody (anti-.mu.) induces resting B cells to proliferation but not differentiation. Upon addition of both LPS and anti-.mu. to cultures, resting B cells again proliferate but do not differentiate. RNA transfer blots of the Ig mRNA 2 days after induction with LPS/anti-.mu. show a specific deficiency of the 2.4-kilobase(kb) .mu. secretory mRNA, whereas the levels of the 2.7-kb .mu. membrane and 1.2-kb .kappa. light chain mRNAs are as high as in cells treated with LPS alone. Between days 3 and 4 after treatment with both reagents, reductions of .mu. membrane and, to a smaller extent, .kappa. mRNA become apparent. As measured by nuclear run-on transcription experiments at day 2, the transcription rates of Ig .mu. and the Ig .kappa. transcription units are equal in both induction experiments. Only at later stages do the LPS/anti-.mu.-treated cells transcribe Ig genes at a lower rate. Thus, the anti-.mu. treatment, drastically reducing the .mu. secretory mRNA production at early stages, represents a negative regulation occurring primarily at the posttranscriptional level.