Biotin. Its place in evolution.

C M Visser; R M Kellogg

doi:10.1007/bf01733892

Home/Archive/PubMed

PubMed · 27642

Biotin. Its place in evolution.

C M Visser·R M Kellogg

View original source ↗Export metadata ↓

Abstract

In the previous article we try to give an explanation for the success of models of enzymatic reactions in which coenzymes play a role. However, one vital cofactor that has thus far not yielded appreciably to this approach is biotin. We attempt to show that biotin presents a fundamentally new sort of problem to bioorganic chemistry; this problem requires consideration both of the origin of life and subsequent evolution in any attempt to understand the anomalies offered by this cofactor.

Explore related subjects

Acetyl-CoA Carboxylase Biological Evolution Biotin Carbon Dioxide Catalysis Enzymes Origin of Life RNA Structure-Activity Relationship Urea Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

C M Visser, R M Kellogg. 1978-06-20. Biotin. Its place in evolution.. https://doi.org/10.1007/bf01733892

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1992

Coordinated regulation and inositol-mediated and fatty acid-mediated repression of fatty acid synthase genes in Saccharomyces cerevisiae.

In Saccharomyces cerevisiae, FAS1, FAS2, and FAS3 are the genes involved in saturated fatty acid biosynthesis. The enzymatic activities of both fatty acid synthase (FAS) and acetyl-CoA carboxylase are reduced 2- to 3-fold when yeast cells are grown in the presence of exogenous fatty acids. The mRNA levels of the FAS genes are correspondingly lower under repressive conditions. Expression of the FAS-lacZ reporter gene is also regulated by fatty acids. When a FAS2 multicopy plasmid is present in the cells, expression of both FAS1 and FAS3 increases. Thus, the FAS genes are coordinately regulated. Deletion analyses of the regulatory regions of FAS1 and FAS2 revealed common regulatory sequences. These include the GGCCAAAAAC and AGCCAAGCA sequences that have a common GCCAA core sequence and the UASINO (upstream activation sequence). Derepression of the FAS genes in the absence of exogenous inositol is not observed when UASINO is mutated, indicating that this cis element is a positive regulator of these genes. The GCCAA elements and UASINO act synergistically for optimal expression of the FAS genes.

Acetyl-CoA Carboxylase↗

PubMed1992

Inhibition of hormone-sensitive lipase by intermediary lipid metabolites.

Hormone-sensitive lipase (HSL) is inhibited in a non-competitive manner by oleoyl CoA, oleic acid and 2-monopalmitoylglycerol, 50% inhibition being observed at concentrations of approx. 0.1 microM, 0.5 microM and 500 microM, respectively. HSL is a key enzyme in lipid metabolism, mobilising triacylglycerol and cholesterol ester stores in several tissues. Feedback inhibition of HSL by oleoyl CoA and oleic acid may therefore prevent accumulation of free fatty acids and cholesterol in the cell, whereas 2-monoacylglycerol may act as a feedback inhibitor if the capacity of monoacylglycerol lipase is exceeded.

Acetyl-CoA Carboxylase↗

PubMed1992

Effect of diets rich in medium-chain and long-chain triglycerides on lipogenic-enzyme gene expression in liver and adipose tissue of the weaned rat.

The activity and mRNA concentrations of two lipogenic enzymes, fatty-acid synthase and acetyl-CoA carboxylase were measured in the liver and white adipose tissue of rats weaned to a carbohydrate-rich diet containing either long-chain or medium-chain fatty acids, and compared to those of rats weaned on a diet containing less than 1% (total energy) fat (high-carbohydrate diet). In the liver, the diet containing long-chain fatty acids inhibited the increase of both lipogenic-enzyme mRNA concentrations and activities seen at weaning on the high-carbohydrate diet but did not prevent the decrease in phosphoenolpyruvate carboxykinase mRNA and activity. In contrast, the diet containing medium-chain fatty acids induced a slower but finally similar increase in lipogenic-enzyme mRNA concentrations and activities. In adipose tissue, a similar trend was observed, although the inhibitory effect of the diet containing long-chain fatty acids was considerably less marked than in liver. It is concluded that medium-chain and long-chain fatty acids have not the same inhibitory potency of the gene expression of lipogenic enzymes, and that long-chain fatty acids have a more marked effect in the liver.

Acetyl-CoA Carboxylase↗