Stable oxygen and carbon isotope composition of benthic foraminifera from the western Mediterranean Sea

The influence of microhabitat, organic matter flux, and metabolism on the stable oxygen and carbon isotope composition of live (Rose Bengal stained) and dead (empty tests) deep-sea benthic foraminifera from the Gulf of Lions (western Mediterranean Sea) have been studied. The total range of observed foraminiferal isotope values exceeds 1.0 per mil for d18O and 2.2 per mil for d13C demonstrating a wide range of coexisting disequilibria relative to d18O of equilibrium calcite (d18OEQ) and d13C of bottom water dissolved inorganic carbon (d13CDIC). The mean d18O values reveal strongest disequilibria for the studied epifaunal to shallow infaunal species (Cibicidoides pachydermus, Uvigerina mediterranea, Uvigerina peregrina) while values approach equilibrium in deep infaunal species (Globobulimina affinis, Globobulimina pseudospinescens). The mean d13C values decrease with increasing average living depths of the different species, thus reflecting a dominant microhabitat (pore water) signal. At the axis of the Lacaze-Duthier Canyon a minimum d13CDIC pore water gradient of approximately -2.1 per mil is assessed for the upper 6 cm of the surface sediment. Although live individuals of U. mediterranea were found in different depth intervals their mean d13C values are consistent with calcification at an average living depth around 1 cm. The deep infaunal occurrence of U. mediterranea specimens suggests association with macrofaunal burrows creating a microenvironment with geochemical characteristics similar to the topmost centimeter. This also explains the excellent agreement between stable isotope signals of live and dead individuals. The ontogenetic enrichment in both d18O and d13C values of U. mediterranea suggests a slow-down of metabolic rates during test growth similar to that previously observed in planktic foraminifera. Enhanced organic carbon fluxes and higher proportion of resuspended terrestrial organic material at the canyon axis are reflected by d13C values of U. mediterranea on average 0.58 per mil lower than those from the open slope. These results demonstrate the general applicability of the d13C signal of this species for the reconstruction of past organic matter fluxes in the Mediterranean Sea. Further studies on live specimens are needed for a more quantitative paleoceanographic approach.

Seawater carbonate chemistry and processes during experiments with amphipod Gammarus locusta, 2009

We report an investigation of the effects of increases in pCO2 on the survival, growth and molecular physiology of the neritic amphipod Gammarus locusta which has a cosmopolitan distribution in estuaries. Amphipods were reared from juvenile to mature adult in laboratory microcosms at three different levels of pH in nominal range 8.1-7.6. Growth rate was estimated from weekly measures of body length. At sexual maturity the amphipods were sacrificed and assayed for changes in the expression of genes coding for a heat shock protein (hsp70 gene) and the metabolic enzyme glyceraldehyde-3-phosphate dehydrogenase (gapdh gene). The data show that the growth and survival of this species is not significantly impacted by a decrease in sea water pH of up to 0.5 units. Quantitative real-time PCR analysis indicated that there was no significant effect of growth in acidified sea water on the sustained expression of the hsp70 gene. There was a consistent and significant increase in the expression of the gapdh gene at a pH of ~7.5 which, when combined with observations from other workers, suggests that metabolic changes may occur in response to acidification. It is concluded that sensitive assays of tissue physiology and molecular biology should be routinely employed in future studies of the impacts of sea water acidification as subtle effects on the physiology and metabolism of coastal marine species may be overlooked in conventional gross "end-point" studies of organism growth or mortality.

Increased feeding and nutrient excretion of adult antarctic krill, Euphausia superba, exposed to enhanced carbon dioxide (CO2)

Ocean acidification has a wide-ranging potential for impacting the physiology and metabolism of zooplankton. Sufficiently elevated CO2 concentrations can alter internal acid-base balance, compromising homeostatic regulation and disrupting internal systems ranging from oxygen transport to ion balance. We assessed feeding and nutrient excretion rates in natural populations of the keystone species Euphausia superba (Antarctic krill) by conducting a CO2 perturbation experiment at ambient and elevated atmospheric CO2 levels in January 2011 along the West Antarctic Peninsula (WAP). Under elevated CO2 conditions (~672 ppm), ingestion rates of krill averaged 78 µg C/individual/d and were 3.5 times higher than krill ingestion rates at ambient, present day CO2 concentrations. Additionally, rates of ammonium, phosphate, and dissolved organic carbon (DOC) excretion by krill were 1.5, 1.5, and 3.0 times higher, respectively, in the high CO2 treatment than at ambient CO2 concentrations. Excretion of urea, however, was ~17% lower in the high CO2 treatment, suggesting differences in catabolic processes of krill between treatments. Activities of key metabolic enzymes, malate dehydrogenase (MDH) and lactate dehydrogenase (LDH), were consistently higher in the high CO2 treatment. The observed shifts in metabolism are consistent with increased physiological costs associated with regulating internal acid-base equilibria. This represents an additional stress that may hamper growth and reproduction, which would negatively impact an already declining krill population along the WAP.

Influence of body mass and skinfolds on skin temperature through infrared thermography

Thermal response of skin temperature (Tsk) has been studied during exercise and immediately after (Merla, 2010). However, more studies about the influence of exercise on Tsk through the time are required to understand the impact of physical activity on thermoregulatory system and metabolism

Mahogany (mg) stimulates feeding and increases basal metabolic rate independent of its suppression of agouti

The mahogany (mg) locus originally was identified as a recessive suppressor of agouti, a locus encoding a skin peptide that modifies coat color by antagonizing the melanocyte-stimulating hormone receptor or MC1-R. Certain dominant alleles of agouti cause an obesity syndrome when ectopic expression of the peptide aberrantly antagonizes the MC4-R, a related melanocyte-stimulating hormone receptor expressed in hypothalamic circuitry and involved in the regulation of feeding behavior and metabolism. Recent work has demonstrated that mg, when homozygous, blocks not only the ability of agouti to induce a yellow coat color when expressed in the skin of the lethal yellow mouse (AY), but also the obesity resulting from ectopic expression of agouti in the brain. Detailed analysis of mg/mg AY/a animals, presented here, demonstrates that mg/mg blocks the obesity, hyperinsulinemia, and increased linear growth induced by ectopic expression of the agouti peptide. Remarkably, however, mg/mg did not reduce hyperphagia in the AY/a mouse. Furthermore, mg/mg induced hyperphagia and an increase in basal metabolic rate in the C57BL/6J mouse in the absence of AY. Consequently, although mahogany is broadly required for agouti peptide action, it also appears to be involved in the control of metabolic rate and feeding behavior independent of its suppression of agouti.

The increased level of β1,4-galactosyltransferase required for lactose biosynthesis is achieved in part by translational control

β1,4-Galactosyltransferase (β4GalT-I) participates in both glycoconjugate biosynthesis (ubiquitous activity) and lactose biosynthesis (mammary gland-specific activity). In somatic tissues, transcription of the mammalian β4GalT-I gene results in a 4.1-kb mRNA and a 3.9-kb mRNA as a consequence of initiation at two start sites separated by ≈200 bp. In the mammary gland, coincident with the increased β4GalT-I enzyme level (≈50-fold) required for lactose biosynthesis, there is a switch from the 4.1-kb start site to the preferential use of the 3.9-kb start site, which is governed by a stronger tissue-restricted promoter. The use of the 3.9-kb start site results in a β4GalT-I transcript in which the 5′- untranslated region (UTR) has been truncated from ≈175 nt to ≈28 nt. The 5′-UTR of the 4.1-kb transcript [UTR(4.1)] is predicted to contain extensive secondary structure, a feature previously shown to reduce translational efficiency of an mRNA. In contrast, the 5′-UTR of the 3.9-kb mRNA [UTR(3.9)] lacks extensive secondary structure; thus, this transcript is predicted to be more efficiently translated relative to the 4.1-kb mRNA. To test this prediction, constructs were assembled in which the respective 5′-UTRs were fused to the luciferase-coding sequence and enzyme levels were determined after translation in vitro and in vivo. The luciferase mRNA containing the truncated UTR(3.9) was translated more efficiently both in vitro (≈14-fold) and in vivo (3- to 5-fold) relative to the luciferase mRNA containing the UTR(4.1). Consequently, in addition to control at the transcriptional level, β4GalT-I enzyme levels are further augmented in the lactating mammary gland as a result of translational control.

Parkinson disease: A new link between monoamine oxidase and mitochondrial electron flow

Two factors that contribute to the progression of Parkinson disease are a brain defect in mitochondrial respiration and the generation of hydrogen peroxide (H2O2) by monoamine oxidase (MAO). Here we show that the two are linked. Metabolism of the neurotransmitter dopamine, or other monoamines (benzylamine, tyramine), by intact rat brain mitochondria suppresses pyruvate- and succinate-dependent electron transport. MAO inhibitors prevent this action. Mitochondrial damage is also reversed during electron flow. A probable explanation is that MAO-generated H2O2 oxidizes glutathione to glutathione disulfide (GSSG), which undergoes thiol-disulfide interchange to form protein mixed disulfides, thereby interfering reversibly with thiol-dependent enzymatic function. In agreement with this premise, direct addition of GSSG to mitochondria resulted in similar reversible inhibition of electron transport. In addition, the monoamines induced an elevation in protein mixed disulfides within mitochondria. These observations imply that (i) heightened activity and metabolism of neurotransmitter by monoamine neurons may affect neuronal function, and (ii) apparent defects in mitochondrial respiration associated with Parkinson disease may reflect, in part, an established increase in dopamine turnover. The experimental results also target mitochondrial repair mechanisms for further investigation and may, in time, lead to newer forms of therapy.

Hormonal prevention of breast cancer: Mimicking the protective effect of pregnancy

Full term pregnancy early in life is the most effective natural protection against breast cancer in women. Rats treated with chemical carcinogen are similarly protected by a previous pregnancy from mammary carcinogenesis. Proliferation and differentiation of the mammary gland does not explain this phenomenon, as shown by the relative ineffectiveness of perphenazine, a potent mitogenic and differentiating agent. Here, we show that short term treatment of nulliparous rats with pregnancy levels of estradiol 17β and progesterone has high efficacy in protecting them from chemical carcinogen induced mammary cancers. Because the mammary gland is exposed to the highest physiological concentrations of estradiol and progesterone during full term pregnancy, it is these elevated levels of hormones that likely induce protection from mammary cancer. Thus, it appears possible to mimic the protective effects of pregnancy against breast cancer in nulliparous rats by short term specific hormonal intervention.

Mouse Deformed epidermal autoregulatory factor 1 recruits a LIM domain factor, LMO-4, and CLIM coregulators

Nuclear LIM domains interact with a family of coregulators referred to as Clim/Ldb/Nli. Although one family member, Clim-2/Ldb-1/Nli, is highly expressed in epidermal keratinocytes, no nuclear LIM domain factor is known to be expressed in epidermis. Therefore, we used the conserved LIM-interaction domain of Clim coregulators to screen for LIM domain factors in adult and embryonic mouse skin expression libraries and isolated a factor that is highly homologous to the previously described LIM-only proteins LMO-1, -2, and -3. This factor, referred to as LMO-4, is expressed in overlapping manner with Clim-2 in epidermis and in several other regions, including epithelial cells of the gastrointestinal, respiratory and genitourinary tracts, developing cartilage, pituitary gland, and discrete regions of the central and peripheral nervous system. Like LMO-2, LMO-4 interacts strongly with Clim factors via its LIM domain. Because LMO/Clim complexes are thought to regulate gene expression by associating with DNA-binding proteins, we used LMO-4 as a bait to screen for such DNA-binding proteins in epidermis and isolated the mouse homologue of Drosophila Deformed epidermal autoregulatory factor 1 (DEAF-1), a DNA-binding protein that interacts with regulatory sequences first described in the Deformed epidermal autoregulatory element. The interaction between LMO-4 and mouse DEAF-1 maps to a proline-rich C-terminal domain of mouse DEAF-1, distinct from the helix–loop–helix and GATA domains previously shown to interact with LMOs, thus defining an additional LIM-interacting domain.