Diauxic Growth of Azotobacter vinelandii on Galactose and Glucose: Regulation of Glucose Transport by Another Hexose

The growth curve of Azotobacter vinelandii was biphasic when the organism was grown in a medium containing a mixture of galactose and glucose. Galactose was the primary carbon source; glucose was also consumed, but the rate at which it was consumed was lower than the rate at which galactose was consumed during the first phase of growth. Metabolic pathways for both sugars were induced. Cell cultures exhibited a second lag period as galactose was depleted. The length of this lag phase varied from 2 to 10 h depending on the pregrowth history of the cells. The second log growth phase occurred at the expense of the remaining glucose in the medium and was accompanied by induction of the high-maximum rate of metabolism glucose-induced glucose permease and increases in the levels of glucose metabolic enzymes. The second lag phase of diauxie may have been due to the time required for induction of the glucose-induced glucose permease.     

A Pressure-dependent Model for the Regulation of Lipoprotein Lipase by Apolipoprotein C-II

Apolipoprotein C-II (apoC-II) is the co-factor for lipoprotein lipase (LPL) at the surface of triacylglycerol-rich lipoproteins. LPL hydrolyzes triacylglycerol, which increases local surface pressure as surface area decreases and amphipathic products transiently accumulate at the lipoprotein surface. To understand how apoC-II adapts to these pressure changes, we characterized the behavior of apoC-II at multiple lipid/water interfaces. ApoC-II adsorption to a triacylglycerol/water interface resulted in large increases in surface pressure. ApoC-II was exchangeable at this interface and desorbed on interfacial compressions. These compressions increase surface pressure and mimic the action of LPL. Analysis of gradual compressions showed that apoC-II undergoes a two-step desorption, which indicates that lipid-bound apoC-II can exhibit at least two conformations. We characterized apoC-II at phospholipid/triacylglycerol/water interfaces, which more closely mimic lipoprotein surfaces. ApoC-II had a large exclusion pressure, similar to that of apoC-I and apoC-III. However, apoC-II desorbed at retention pressures higher than those seen with the other apoCs. This suggests that it is unlikely that apoC-I and apoC-III inhibit LPL via displacement of apoC-II from the lipoprotein surface. Upon rapid compressions and re-expansions, re-adsorption of apoC-II increased pressure by lower amounts than its initial adsorption. This indicates that apoC-II removed phospholipid from the interface upon desorption. These results suggest that apoC-II regulates the activity of LPL in a pressure-dependent manner. ApoC-II is provided as a component of triacylglycerol-rich lipoproteins and is the co-factor for LPL as pressure increases. Above its retention pressure, apoC-II desorbs and removes phospholipid. This triggers release of LPL from lipoproteins.     

Evidence for a Role of the Transcriptional Regulator Maid in Tumorigenesis and Aging

Maid is a helix-loop-helix protein that is involved in cell proliferation. In order to further elucidate its physiological functions, we studied Maid activity in two small fish model systems. We found that Maid expression was greatest in zebrafish liver and that it increased following partial hepatectomy. Maid levels were also high in hepatic preneoplastic foci induced by treatment of zebrafish with diethylnitrosamine (DEN), but low in hepatocellular carcinomas (HCC), mixed tumors, and cholangiocarcinomas developing in these animals. In DEN-treated transgenic medaka overexpressing Maid, hepatic BrdU uptake and proliferation were reduced. After successive breedings, Maid transgenic medaka exhibited decreased movement and a higher incidence of abnormal spine curvature, possibly due to the senescence of spinal cord cells. Taken together, our results suggest that Maid levels can influence the progression of liver cancer. In conclusion, we found that Maid is important regulator of hepatocarconogenesis and aging.     

Regulation of Iron Homeostasis in Arabidopsis thaliana by the Clock Regulator Time for Coffee

In plants, iron homeostasis is tightly regulated to supply sufficient amounts of this metal for an optimal growth while preventing excess accumulation to avoid oxidative stress. To identify new regulators of iron homeostasis, a luciferase-based genetic screen using the Arabidopsis AtFer1 ferritin promoter as a target was developed. This screen identified TIME FOR COFFEE (TIC) as a regulator of AtFer1 gene expression. TIC was previously described as a nuclear regulator of the circadian clock. Mutants in the TIC gene exhibited a chlorotic phenotype rescued by exogenous iron addition and are hypersensitive to iron during the early stages of development. We showed that iron overload-responsive genes are regulated by TIC and by the central oscillator of the circadian clock. TIC represses their expression under low iron conditions, and its activity requires light and light/dark cycles. Regarding AtFer1, this repression is independent of the previously characterized cis-acting element iron-dependent regulatory sequence, known to be involved in AtFer1 repression. These results showed that the regulation of iron homeostasis in plants is a major output of the TIC- and central oscillator-dependent signaling pathways.     

Transcriptional Regulation by Pho23 Modulates the Frequency of Autophagosome Formation

1. Download : Download high-res image (384KB)
2. Download : Download full-size image