Murine plasmacytomas constitute a class of natural heat-shock variants in which the major inducible hsp-68 gene is not expressed.

Abstract

Analysis of the heat-shock response in murine plasmacytomas reveals that, as demonstrated previously for the MPC-11 cell line, the genes coding for the 68-kilodalton heat-shock protein (hsp-68) are not expressed upon heat shock or sodium arsenite treatment. Noninduction is unique to the normally coordinated set of three hsp-68 genes since at least two other heat-shock protein genes (hsp-70 and hsp-89) are properly induced. No other lymphoid cell line was found to possess silent hsp-68 genes. Cell lines examined included a T lymphoma, a pre-B lymphocyte, and a non-B-non-T tumor cell line, as well as an Ig-nonproducing myeloma of undetermined differentiated status. Nonexpression is strain-independent as observed in BALB/c and C3H plasmacytomas. Based on S1 nuclease analysis using a cloned genomic hsp-68 probe, nonexpression is caused by the absence of hsp-68 mRNA following heat shock. A time-course experiment suggests that rapid degradation of mRNA does not occur, implying that the block is most likely at the transcriptional level. Southern blot analysis does not indicate any minor deletions around the region of transcription initiation, at least in the probed hsp-68 gene. These results suggest that the absence of hsp-68 gene expression may be a reflection of the differentiated and (or) transformed state of murine plasma cells, possibly through the absence or deregulation of a regulatory factor required for induction of heat-shock genes.