Homology of Drosophila yolk proteins and the triacylglycerol lipase family

Drosophila yolk proteins consist of a set of related proteins of 50,000 Mr. They are derived from slightly larger precursors by cleavage of a signal peptide. In this respect, they differ from the yolk proteins of other insects which are proteolytic fragments of precursors of 200,000 Mr or larger, termed vitellogenins and probably homologous to the vitellogenins of other egg-laying species. We report here a comparative amino acid analysis demonstrating that the Drosophila yolk proteins are non-homologous to the vitellogenin group of yolk proteins, but surprisingly are related to the triacylglycerol lipase family.     

Evolution of major metabolic innovations in the Precambrian

A combination of the information on the metabolic capabilities of prokaryotes with a composite phylogenetic tree depicting an overview of prokaryote evolution based on the sequences of bacterial ferredoxin, 2Fe–2S ferredoxin, 5S ribosomal RNA, andc-type cytochromes shows three zones of major metabolic innovation in the Precambrian. The middle of these, which reflects the genesis of oxygenreleasing photosynthesis and aerobic respiration, links metabolic innovations of the anaerobic stem on the one hand and, on the other, proliferation of aerobic bacteria and the symbiotic associations leading to the eukaryotes. We consider especially those pathways where information on the structure of the enzymes is known.Halobacterium andThermoplasma (archaebacteria) do not belong to a totally independent line on the basis of the composite tree but branch from the eukaryote cytoplasmic line.     

Molecular phylogeny of Rodentia in the descent of genusBandicota

The interrelationships of murids and other rodent families as well as the evolutionary descent of multiple β-globins of murines are deduced from parsimony trees of relevant globin sequences. Our results show that Caviidae arises first, followed by Sciuridae which joins Muridae. In the murid line of descent Spalacinae arises first followed by two branches, one representing Cricentinae and Arvicolinae and the other Murinae. Although the rates of evolution of globin genes in the different rodent families are different, the murid branches show more or less a uniform rate of evolution of β globins. We have used this information to show that mouse-rat divergence occurred around 20 million years ago. The evolutionary rationale for the presence and the expression of different β-globin genes in murid populations is also discussed. Based on mitochondrial DNA restriction fragment analysis, the between-species relationships ofRattus rattus rufescens, Bandicota indica andBandicota bengalensis have been assessed and the time of divergence of the two bandicoot rats estimated.     

Effects of fecal age and seasonality on steroid hormone concentration as a reproductive parameter in field studies

We studied how fecal age (6, 12, 24, 48, 72, and 168 h) and seasonality affect variation in the fecal steroid hormone metabolite concentration in three endangered mammalian species, Mhorr gazelle, Saharan Barbary sheep, and the Iberian lynx. Except for estrogens, concentrations remained stable for at least 48 h in the Mhorr gazelle and the Saharan Barbary sheep. Steroid hormone metabolite concentration remained stable in the Iberian lynx throughout the experiment (1 week). Seasonality was the main factor affecting variation in hormone metabolite concentrations, and although the response was species- and hormone-specific, the dry season resulted in increased hormone metabolite concentrations, while the wet season reduced the concentration.     

Spectinomycin resistance mutations in the rrn16 gene are new plastid markers in Medicago sativa

We report here the isolation of spectinomycin-resistant mutants in cultured cells of Medicago sativa line RegenSY-T2. Spectinomycin induces bleaching of cultured alfalfa cells due to inhibition of protein synthesis on the prokaryotic type 70S plastid ribosomes. Spontaneous mutants resistant to spectinomycin bleaching were identified by their ability to form green shoots on plant regeneration medium containing selective spectinomycin concentrations in the range of 25–50?mg/l. Sequencing of the plastid rrn16 gene revealed that spectinomycin resistance is due to mutations in a conserved stem structure of the 16S rRNA. Resistant plants transferred to the greenhouse developed normally and produced spectinomycin-resistant seed progeny. In light of their absence in soybean, a related leguminous plant, the isolation of spectinomycin-resistant mutants in M. sativa was unexpected. The new mutations are useful for the study of plastid inheritance, as demonstrated by detection of predominantly paternal plastid inheritance in the RegenSY-T2?×?Szapko57 cross, and can be used as selective markers in plastid transformation vectors to obtain cisgenic plants.     

Mechano-induced cell metabolism promotes microtubule glutamylation to force metastasis

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Effect of an acute moderate‐exercise session on metabolic and inflammatory profile of PPAR‐α knockout mice

Peroxisome proliferator‐activated receptors (PPARs) play a major role in metabolism and inflammatory control. Exercise can modulate PPAR expression in skeletal muscle, adipose tissue, and macrophages. Little is known about the effects of PPAR‐α in metabolic profile and cytokine secretion after acute exercise in macrophages. In this context, the aim of this study was to understand the influence of PPAR‐α on exercise‐mediated immune metabolic parameters in peritoneal macrophages. Mice C57BL/6 (WT) and PPAR‐α knockout (KO) were examined in non‐exercising control (n = 4) or 24 hours after acute moderate exercise (n = 8). Metabolic parameters (glucose, non‐esterified fatty acids, total cholesterol [TC], and triacylglycerol [TG]) were assessed in serum. Cytokine concentrations (IL‐1β, IL‐6, IL‐10, TNF‐α, and MCP‐1) were measured from peritoneal macrophages cultured or not with LPS (2.5 μg/mL) and Rosiglitazone (1 μM). Exercised KO mice exhibited low glucose concentration and higher TC and TG in serum. At baseline, no difference in cytokine production between the genotypes was observed. However, IL‐1β was significantly higher in KO mice after LPS stimulus. IL‐6 and IL‐1β had increased concentrations in KO compared with WT, even after exercise. MCP‐1 was not restored in exercised KO LPS group. Rosiglitazone was not able to reduce proinflammatory cytokine production in KO mice at baseline level or associated with exercise. Acute exercise did not alter mRNA expression in WT mice. Conclusion: PPAR‐α seems to be needed for metabolic glucose homeostasis and anti‐inflammatory effect of acute exercise. Its absence may induce over‐expression of pro‐inflammatory cytokines in LPS stimulus. Moreover, moderate exercise or PPAR‐γ agonist did not reverse this response.     

The Budding Yeast Ubiquitin Protease Ubp7 Is a Novel Component Involved in S Phase Progression

DNA damage must be repaired in an accurate and timely fashion to preserve genome stability. Cellular mechanisms preventing genome instability are crucial to human health because genome instability is considered a hallmark of cancer. Collectively referred to as the DNA damage response, conserved pathways ensure proper DNA damage recognition and repair. The function of numerous DNA damage response components is fine-tuned by posttranslational modifications, including ubiquitination. This not only involves the enzyme cascade responsible for conjugating ubiquitin to substrates but also requires enzymes that mediate directed removal of ubiquitin. Deubiquitinases remove ubiquitin from substrates to prevent degradation or to mediate signaling functions. The Saccharomyces cerevisiae deubiquitinase Ubp7 has been characterized previously as an endocytic factor. However, here we identify Ubp7 as a novel factor affecting S phase progression after hydroxyurea treatment and demonstrate an evolutionary and genetic interaction of Ubp7 with DNA damage repair pathways of homologous recombination and nucleotide excision repair. We find that deletion of UBP7 sensitizes cells to hydroxyurea and cisplatin and demonstrate that factors that stabilize replication forks are critical under these conditions. Furthermore, ubp7Δ cells exhibit an S phase progression defect upon checkpoint activation by hydroxyurea treatment. ubp7Δ mutants are epistatic to factors involved in histone maintenance and modification, and we find that a subset of Ubp7 is chromatin-associated. In summary, our results suggest that Ubp7 contributes to S phase progression by affecting the chromatin state at replication forks, and we propose histone H2B ubiquitination as a potential substrate of Ubp7.