Changes of mitochondrial NADH₂ oxidation pathways in Torulopsis utilis grown on acetate

Factors controlling the occurrence of site I phosphorylation in C. utilis mitochondria

“…Therefore the by-pass mechanism of Site I phosphorylation in mitochondria can be distinguished from the intrinsic effect of iron deficiency which causes the lack of energy transducing component(s) at Site I. In this connection Fukami et al [9] have reported that acetate-limited growth of C. utilis cells results in the loss of the external rotenone insensitive NADH dehydrogenase. It was found, however, that in the culture medium containing acetate as a main carbon source C. utilis can grow exponentially only in the medium with pH higher than around 5.5.…”

“…Under these sub-optimal growth conditions, acetate respiration of the cells exhibits piericidin A sensitivity, even when cells are growing with excess carbon source and with excess oxygen supply. This explains the inability of C. utilis cells to grow in acetateculture medium (pH 5.0), which contains piericidin A or rotenone [9].…”

A comparison of mitochondria from Torulopsis utilis grown in continous culture with glycerol, iron, ammonium, magnesium or phosphate as the growth-limiting nutrient

“…For growth limited by glycerol, NH4+, Mg2+, phosphate, iron or SO42-, the pH of the culture tended to fall and 2M-KOH was added automatically whenever the pH fell below 5.0. When growth was limited by acetate (as the sodium salt; Fukami, Light & Garland, 1970), the pH of the culture tended to rise and the correct controlling action was achieved by reversing the connexions to the inputs of amplifier A3 and substituting 2m-HCI for KOH.…”

Biochemical applications of continuous culture: energy-conservation mechanisms in Torulopsis utilis

“…The reasons for this insensitivity have been discussed elsewhere (Garland et al 1969), and were thought to involve the presence of an externally orientated NADH dehydrogenase that calaysed a rotenone-insensitive oxidation of extramitochondrial NADH . Recently Dr M. Fukami has shown in our laboratory that growth of T. utilis on acetate represses the external NADH dehydrogenase of mitochondria (Fukami, Light & Garland, 1970). Both respiration and growth of whole cells were highly sensitive to rotenone and piericidin A provided that the carbon source was acetate, and screening for resistant mutants now poses no difficulty (P. A.…”