Fig. 6.

Effect of 60 min of restraint stress on pro-apoptotic mRNA expression in the testes. In bats exposed to restraint (n=8) there was a significant transcriptional upregulation of (A) Bax and (B) cytochrome c, but not (C) Apaf-1 mRNA expression relative to control animals (n=8; *P<0.05). Bar plots represent means±s.e.m., with individual expression depicted within each group by circles to highlight interindividual variation and range. (D) These target molecules are involved in a mitochondria-mediated pro-apoptotic pathway that begins with activation of death receptors in the cell membrane. This signal of cellular stress stimulates Bid and Bim to activate Bax, which then dimerizes and induces mitochondrial membrane permeabilization and subsequent release of cytochrome c from the outer mitochondrial matrix. Cytochrome c binds to Apaf-1, permitting the interaction of Apaf-1 with caspase-9. Activation of caspase-9 is the first in a series of classical downstream caspase activation steps that ultimately leads to cellular apoptosis.