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pubmed:abstractText |
A genetically determined malfunction of energy conservation reduces assimilation of substrate to half or less its normal level while leaving oxidative processes apparently unchanged. This metabolic defect, which differs in many ways from any previously described, is related to the function of the B incompatibility factor and occurs both in the common A heterokaryon (A = B not equal)-in which two compatible, wild B factors interact-and in mutant-B homokaryons.
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