HSP12, a new small heat shock gene of Saccharomyces cerevisiae: Analysis of structure, regulation and function

Summary We have isolated a new small heat shock gene, HSP12, from Saccharomyces cerevisiae. It encodes a polypeptide of predicted Mr 12 kDa, with structural similarity to other small heat shock proteins. HSP12 gene expression is induced several hundred-fold by heat shock and on entry into stationary phase. HSP12 mRNA is undetectable during exponential growth in rich medium, but low levels are present when cells are grown in minimal medium. Analysis of HSP12 expression in mutants affected in cAMP-dependent protein phosphorylation suggests that the gene is regulated by cAMP as well as heat shock. A disruption of the HSP12 coding region results in the loss of an abundant 14.4 kDa protein present in heat shocked and stationary phase cells. It also leads to the induction of the heat shock response under conditions normally associated with low-level HSP12 expression. The HSP12 disruption has no observable effect on growth at various temperatures, nor on the ability to acquire thermotolerance.     

Growth versus molting time of caterpillars as a function of temperature,nutrient concentration and the phenolic rutin

Summary A factorial experiment tested the effects of varying nutrient concentration (normal versus diluted), presence or absence of the phenolic allelochemical rutin and daytime temperature (20, 25 and 30° C) on growth, molting and food utilization efficiencies of tobacco hornworms (Manduca sexta). Two of the utilization efficiencies (approximate digestibility and efficiency of conversion of ingested food) were unaffected by temperature; the third one, efficiency of conversion of digested food, was affected by temperature but there was no consistent effect. Lower temperatures significantly increased the proportion of the stadium spent molting, with larvae at a daytime temperature of 20° C spending 9% more of the stadium in molting than larvae at 30° C. Growth time was not influenced by nutrient concentration. When temperature was low and rutin absent, molt time and the proportion of the stadium spent molting were affected by nutrient concentration. Addition of the phenolic rutin did not have an appreciable effect on growth time or digestive processes. However, it increased molting time by 7 to 14% and thus increased the duration of the stadium and reduced relative growth rate. These results indicate that the effect of food quality on growth rate is a function of the thermal conditions of insect herbivores. At cooler temperatures, a disproportionate increase in time spent molting, rather than altered food utilization efficiencies, contributed to lower growth rates. The consequences for larval growth of fluctuating temperatures due to diurnal cycles and the presence of predators forcing larvae into thermally suboptimal microhabitats are discussed.     

Down''s Syndrome Individuals Begin Life with Normal Levels of Brain Cholinergic Markers

We measured the activities of the cholinergic marker enzymes choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) in autopsied brains of seven infants (age range 3 months to 1 year) with Down's syndrome (DS), a disorder in which virtually all individuals will develop by middle age the neuropathological changes of Alzheimer's disease accompanied by a marked brain cholinergic reduction. When compared with age-matched controls cholinergic enzyme activity was normal in all brain regions of the individuals with infant DS with the exception of above-normal activity in the putamen (ChAT) and the occipital cortex (AChE). Our neurochemical observations suggest that DS individuals begin life with a normal complement of brain cholinergic neurons. This opens the possibility of early therapeutic intervention to prevent the development of brain cholinergic changes in patients with DS.     

Phenology of Festuca pallescens in relation to topography in north-western Patagonia

Abstract. The phenological changes in populations of Festuca pallescens (St. Yves) Parodi at different topographic positions and exposure along an altitudinal gradient (600 - 1100 m) were investigated during two growing seasons in northwestern Patagonia. Stepwise multiple regression analysis was used to describe the relationship between phenology and environment during the entire growing season. Analysis of variance was also performed at each sample date to detect significant environmental factors influencing phenology at different sites. The sum of maximum air temperatures was identified as the environmental variable best correlated with the seasonal variation of phenological events of Festuca pallescens over the period of two growing seasons, explaining 93.2 % of the total variance. Significant differences between sites were observed at each sample date. Main effects of altitude and topographic position and two-way interactions between altitude and topographic position, and topographic position and exposure were also detected as significant. Phenology was delayed at increased altitude. Differences in phenology between topographic sites at the same altitude were not detected during the entire growing season and were only observed in the reproductive phase. At this time, the phenology was significantly delayed at high topographic positions on the slopes as compared with low and mid positions. At high altitudes in the valley (950 m a. s. 1.), where steep slopes and humid conditions prevail, phenology was delayed on western exposures and low positions. The results adequately summarize and quantify the effect of spatial and temporal environmental variation on the phenological development of Festuca pallescens in northwestern Patagonia.     

Regional Reductions of Transketolase in Thiamine-Deficient Rat Brain

Abstract: Thiamine deficiency impairs oxidative metabolism and causes metabolic encephalopathy. An early reduction in transketolase (TK) activity may be an important pathogenic event. To assess the role of TK, we have delineated the regional/cellular distribution of TK protein and mRNA in adult rat brain in pyrithiamine-induced thiamine deficiency. TK activity declined in both vulnerable and spared regions. Immunoblots showed a parallel reduction of TK protein. With a few exceptions, immunocytochemistry indicated an overall decline of TK immunoreactivity and the decrease was not specific to vulnerable areas. In contrast to the pronounced, general decline of TK protein, in situ hybridization revealed a regional decrease of 0–25% of TK mRNA in thiamine deficiency. Northern blots indicated a similar level of TK mRNA in whole brain in thiamine deficiency. These results show that the decline of TK activity results from a proportional decrease of TK protein, and the deficiency may be due to an instability of TK protein or an inhibition of TK mRNA translation. The lack of correlation of the distribution, and the absence of specific alteration, of TK in affected regions suggest that the reduced TK may not be linked directly to selective vulnerability in thiamine deficiency.     

Ethanol Inhibits Basic Fibroblast Growth Factor-Mediated Proliferation of C6 Astrocytoma Cells

Abstract: Early ethanol exposure alters the proliferative activity of glial and neuronal precursors in the developing CNS. The present study tests the hypothesis that ethanol-induced alterations in cell proliferation result from interference with growth factors. An in vitro model of astroglia (C6 astrocytoma cells) was used to study the effects of ethanol on proliferation mediated by basic fibroblast growth factor (bFGF). bFGF stimulated the proliferation of C6 cells. This bFGF-enhanced proliferation was evident by increases in total cell number, DNA synthesis (as measured by [³H]thymidine incorporation), and the number of cells that took up bromodeoxyuridine. A synthetic peptide that specifically blocked the binding of bFGF to its high-affinity receptor completely abolished the proliferation-promoting effect of bFGF. The action of another mitogen for C6 cells, insulin-like growth factor-1, was not affected by this peptide. Therefore, the bFGF-stimulated proliferation was mediated through a specific bFGF receptor. Ethanol inhibited bFGF-mediated proliferation in a concentration-dependent manner. Ethanol concentrations of 100 and 200 mg/dl partially inhibited bFGF-mediated proliferation (by 58 and 74%, respectively), whereas concentrations of ≥400 mg/dl completely abolished the growth-stimulating effect of bFGF. Our data show that ethanol alters proliferative activity of C6 cells by disrupting the action of bFGF. The target of ethanol neurotoxicity is a receptor-mediated activity. bFGF can affect cell proliferation by a non-receptor-mediated intracellular pathway, but ethanol does not have an impact on this pathway.     

A unique genomic sequence in the Wolf-Hirschhorn syndrome [WHS] region of humans is conserved in the great apes

The Wolf-Hirschhorn syndrome (WHS) is caused by a partial deletion in the short arm of chromosome 4 band 16.3 (4p16.3). A unique-sequence human DNA probe (39 kb) localized within this region has been used to search for sequence homology in the apes' equivalent chromosome 3 by FISH-technique. The WHS loci are conserved in higher primates at the expected position. Nevertheless, a control probe, which detects alphoid sequences of the pericentromeric region of humans, is diverged in chimpanzee, gorilla, and orangutan. The conservation of WHS loci and divergence of DNA alphoid sequences have further added to the controversy concerning human descent.     

Proliferation and Teratogenicity of Aino Virus in Chick Embryos

Aino virus (AIV; JaNAr 28 strain) 10³ TCID₅₀/0.2 ml was inoculated in the yolk sac of 8-day-old chick embryos. Recovery and titration of the virus from various organs including the central nervous system (CNS) and skeletal muscle were performed at 2, 4, 7, 10 and 13 days after inoculation (PI). AIV was systemically disseminated and proliferated even 2 days PI. The titers of the recovered virus from the CNS and from skeletal muscle was the highest at 4 days PI and declined with time, whereas hydranencephaly, arthrogryposis and cerebellar hypoplasia developed at 7 days PI and gradually progressed until 13 days PI.