Mas20p and Mas70p are integral proteins of the yeast mitochondrial outer membrane that appear to function as receptors for precursor proteins imported from the cytosol. Loss of either receptor alone does not block import or kill the cells, but deletion of Mas20p causes loss of respiration (Ramage, L., Junne, T., Hahne, K., Lithgow, T., and Schatz, G. (1993) EMBO J. 12, 4115- 4123). Here we show that this respiratory deficiency is only temporary; given time to adapt, virtually all cells lacking MAS20p regain respiration without regaining MAS20p. The respiratory defect can also be suppressed (at a frequency of about 10-6) by a dominant mutation of a single nuclear gene. The suppressed cells, unlike the unsuppressed ones, tolerate disruption of the MAS70 gene. The resulting double disruptants lack both Mas20p and Mas70p, yet are viable and able to respire. Protein import into mitochondria isolated from these cells is efficient, specific, and highly sensitive to protease treatment. We propose that at least one additional mitochondrial surface protein can function as a protein import receptor and that the activity of this component is up-regulated by a stress response or by an extragenic suppressor.
|Number of pages||6|
|Journal||The Journal of Biological Chemistry|
|Publication status||Published - 27 May 1994|