Such a critical glycolytic demand for ATP
would predictably cause cells to exist in a fragile state, susceptible
to death by even modest transient increases in cell demands for
ATP. In the second scenario, Htt may act in a mitochondria
autonomous manner for coupling of the mitochondrial proton
gradient to ATP generation. If so, the absence of Htt would
limit dissipation of the mitochondrial membrane potential and
thereby promote the viability of cells despite an apparent failure in
mitochondrial ATP synthesis. From the two scenarios we currently
favorthe first