Investigators interested in studying the activation of apoptosis inject cytochrome c into the cytosol of two types of mammalian cells: cells that are normal and cells in which Bak and Bax have been inactivated by mutation. How would these cells be predicted to respond? Question 3 options: The normal cells will undergo apoptosis and the mutant cells will continue to grow. The mutant cells will undergo apoptosis and the normal cells will continue to grow. Neither cell type will undergo apoptosis, so both will continue to grow. The normal cells will undergo apoptosis and the mutant cells will die by necrosis. Both cell types will undergo apoptosis.

Both cell types will undergo aptosis

Explanation:

cells lacking both Bax and Bak, but not cells lacking only one of these components, are completely resistant to tBID-induced cytochrome c release and apoptosis. Moreover, doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin. Thus, activation of a “multidomain” proapoptotic member, BAX or BAK, appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli.

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