Additionally, the examples of the SOS response, prophage excision, and relaxase function suggest targeting of these processes can potentially lead to the accumulation of toxic intermediates and cell death.
Several intermediate forms of cell death have been identified and characterised [ 6, 7], including mitotic catastrophe and autophagic cell death.
Noteworthily, aponecrosis, an intermediate form of cell death sharing the morphological and molecular aspects of apoptosis and necrosis, was shown to abolish any antithesis between these two forms of cell demise.
Additionally, mitochondria are important for calcium homeostasis, oxidative stress processes, production of metabolic intermediates and programmed cell death (PCD).
We have previously shown that compromising the function of the GABA-shunt, by disrupting the SSADH gene of Arabidopsis, causes enhanced accumulation of reactive oxygen intermediates (ROIs) and cell death in response to light and heat stress.
We have previously shown that compromising the function of the GABA-shunt causes enhanced accumulation of reactive oxygen intermediates (ROIs) and cell death in response to light and heat stress [26].
Production of mitochondrial ROS is not only restricted to IR but indeed may be an important intermediate in intrinsic and extrinsic (cell death receptor-dependent) pathways of cell death induction.
The problem of the 'steady state' concentration of reactive intermediates is not academic: reactive intermediates of oxidative stress can induce necrotic cell death, caspase-dependent apoptosis [ 184- 186] or other intermediate forms, including apoptosis-like or necrosis-like cell death [ 96], even in the presence of the same pro-oxidant agent or condition [ 179- 190, 191, 191].
However, in this case deletion of terminal subdomains, or their large parts, would also have to be concurrent, otherwise nonfunctional intermediates could arise, leading to cell death due to insufficient protection against the cognate ENase.
