On the role of intracellular potassium in protein synthesis
On the role of intracellular potassium in protein synthesis.
The stimulatory effect of signaling on metabolic activity and the metabolic rate studies of ; ; ; ) also argue against a hypometabolic effect induced by food restriction. They studied the oxygen consumption and heat production rates of normally fed controls and worms that were restricted by three dietary restriction (DR) protocols: bacterial dilution in liquid culture, axenic liquid culture and the use of Eat mutants. mutations produce defects in pharyngeal pumping that lead to a reduction in food uptake and concomitant DR phenotypes, including a starved appearance, reduced brood size and extended lifespan. Both proxies of metabolic rate remained unchanged or were elevated in restricted worms. Thus food restriction does not act by lowering the rate of metabolism. At first glance the failure to reduce energy expenditure when food is scarce may seem wasteful. One possible explanation is that there is an increased requirement for synthesis of compounds that are otherwise adequately supplied by food. This is consistent with the lower standing levels of ATP measured in young adult (for about the first 5 days of adulthood) worms grown in axenic culture, which induced the strongest DR phenotype. It is not known if DR animals produce more ROS. DR by all three methods increased SOD and catalase activities, and axenic culture effectively enhanced resistance to thermal and oxidative stress. However, these effects may be part of a complex longevity assurance program that can be induced by a number of unfavorable conditions, including DR, rather than a specific response to increased ROS.
Protein synthesis in halophytes: The influence of potassium, ..
Mutations that compromise the function of the mitochondrial electron transport chain might be predicted to shorten the lifespan but, remarkably, such mutations frequently confer lifespan extension (). In a systematic RNAi screen for genes conferring longevity, genes related to mitochondrial function were over-represented tenfold (). Long-lived worms, in which mitochondrial function was disturbed by RNAi, displayed low ATP levels and oxygen consumption rates compared to appropriate controls. These metabolic phenotypes confirmed an earlier study in which the function of several subunits of the electron transport chain complexes I, III, IV and V were compromised by RNAi knockdown (). These animals were small and showed slow development and behavior (pharyngeal pumping and defecation). Small size, however, is not a universal hallmark of mitochondrial mutants. Hypometabolic mutants, which contain a defect in an iron-sulphur protein subunit of complex III, were reported to have a normal body size (). Some mitochondrial mutants of the Clock family, such as (a gene involved in ubiquinone synthesis) (; review by ) and (involved in the efficiency and fidelity of mitochondrial protein synthesis), are not hypometabolic (; ). Indeed, in mutants complex I activity remains unaltered (; ; ), although this was challenged by ) who found that complex I activity was decreased by approximately 70% while complex II activity was left intact when compared to wild type.