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First published online February 12, 2004
doi: 10.1242/10.1242/jcs.00943
Research Article |


Department of Biochemistry, Université de Montréal, Montréal, Québec H3C 3J7, Canada
Author for correspondence (e-mail: luis.rokeach{at}umontreal.ca)
Accepted 16 October 2003
Calnexin is a molecular chaperone playing key roles in protein folding and the quality control of this process in the endoplasmic reticulum. We, and others, have previously demonstrated that cnx1+, the gene encoding the calnexin homologue in Schizosaccharomyces pombe, is essential for viability. We show that a particular cnx1 mutant induces a novel mechanism allowing the survival of S. pombe cells in the absence of calnexin/Cnx1p. Calnexin independence is dominant in diploid cells and is inherited in a non-Mendelian manner. Remarkably, this survival pathway, bypassing the necessity for calnexin, can be transmitted by transformation of cell extracts into a wild-type naive strain, thus implicating a non-chromosomal factor. Nuclease and UV treatments of cells extracts did not obliterate transmission of calnexin independence by transformation. However, protease digestion of extracts did reduce the appearance of calnexin-independent cells, indicating that a protein element is required for calnexin-less viability. We discuss a model in which this calnexin-less survival mechanism would be activated and perpetuated by a protein component acting as a genetic element.
Key words: Non-Mendelian Genetics, Yeast genetics, Protein folding, Fission Yeast
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