Feeding ecology of the common sun skink,Eutropis multifasciata (Reptilia: Squamata: Scincidae), in the plains of central Vietnam

We studied the feeding ecology of Eutropis multifasciata in the tropical plains of central Vietnam to understand better the foraging mode, spatiotemporal and sexual variation in dietary composition, and rarefaction curves of prey-taxon richness for males and females. Stomach contents (n = 161) were collected from October 2013 to May 2014 using a nonlethal stomach-flushing technique. A total of 680 food items (624 animal items and 56 plant items) was found in 161 stomachs of skinks, representing 19 unique animal categories. We found that the diet of E. multifasciata is composed mainly of small, sedentary and clumped prey and that this skink specialises on spiders, insect larvae, snails, grasshoppers and crickets (with a combined importance index of 60%). Dietary composition, prey size and total prey volume in E. multifasciata changed between dry and rainy seasons and among regions. The total volume of food items consumed by males was larger than that of females, and the diversity and evenness index of prey categories were larger in males than in females. However, using rarefaction curves revealed that females have the higher prey-taxon richness after points between 130 and 140 prey items for frequency, and between 160 and 170 prey items for number of items, and the differences were not statistically significant. The foraging behaviour of E. multifasciata best fits a ‘widely foraging’ model.     

Activation of ataxia telangiectasia muted under experimental models and human Parkinson’s disease

In the present study we demonstrated that neurotoxin MPP⁺-induced DNA damage is followed by ataxia telangiectasia muted (ATM) activation either in cerebellar granule cells (CGC) or in B65 cell line. In CGC, the selective ATM inhibitor KU-55933 showed neuroprotective effects against MPP⁺-induced neuronal cell loss and apoptosis, lending support to the key role of ATM in experimental models of Parkinson’s disease. Likewise, we showed that knockdown of ATM levels in neuroblastoma B65 cells using an ATM-specific siRNA attenuates the phosphorylation of retinoblastoma protein without affecting other cell-cycle proteins involved in the G₀/G₁ cell-cycle phase. Moreover, we demonstrated DNA damage, in human brain samples of PD patients. These findings support a model in which MPP⁺ leads to ATM activation with a subsequent DNA damage response and activation of pRb. Therefore, this study demonstrates a new link between DNA damage by MPP⁺ and cell-cycle re-entry through retinoblastoma protein phosphorylation.     

Triosephosphate isomerase: a highly evolved biocatalyst

Triosephosphate isomerase (TIM) is a perfectly evolved enzyme which very fast interconverts dihydroxyacetone phosphate and d-glyceraldehyde-3-phosphate. Its catalytic site is at the dimer interface, but the four catalytic residues, Asn11, Lys13, His95 and Glu167, are from the same subunit. Glu167 is the catalytic base. An important feature of the TIM active site is the concerted closure of loop-6 and loop-7 on ligand binding, shielding the catalytic site from bulk solvent. The buried active site stabilises the enediolate intermediate. The catalytic residue Glu167 is at the beginning of loop-6. On closure of loop-6, the Glu167 carboxylate moiety moves approximately 2 Å to the substrate. The dynamic properties of the Glu167 side chain in the enzyme substrate complex are a key feature of the proton shuttling mechanism. Two proton shuttling mechanisms, the classical and the criss-cross mechanism, are responsible for the interconversion of the substrates of this enolising enzyme.     

The origins and early years of the Magnetic and Meteorological department at Greenwich Observatory, 1834-1848*

As one of his first acts upon becoming Astronomer Royal in 1835, George Airy made moves to set up a new observatory at Greenwich to study the Earth’s magnetic field. This paper uses Airy’s correspondence to argue that, while members of the reform movement in British science were putting pressure on the Royal Observatory to branch out into geomagnetism and meteorology, Airy established the magnetic observatory on his own initiative, ahead of Alexander von Humboldt’s request for British participation in the worldwide magnetic charting project that later became known as the ‘Magnetic Crusade’. That the Greenwich magnetic observatory did not become operational until 1839 was due to a series of incidental factors that provide a case study in the technical and political obstacles to be overcome in building a new government observatory. Airy attached less importance to meteorology than he did to geomagnetism. In 1840, he set up a full programme of meteorological observations at Greenwich – and thus turned his magnetic observatory into the ‘Magnetic and Meteorological department’ – only as the price of foiling an attempt by Edward Sabine and others in the London scientific elite to found a rival magnetic and meteorological observatory. Studying the origins of Airy’s Magnetic and Meteorological department highlights how important the context of other institutions and trends in science is to understanding the development of Britain’s national observatory.     

Hormonal control of Sertoli cell metabolism regulates spermatogenesis

Hormonal regulation is essential to spermatogenesis. Sertoli cells (SCs) have functions that reach far beyond the physical support of germ cells, as they are responsible for creating the adequate ionic and metabolic environment for germ cell development. Thus, much attention has been given to the metabolic functioning of SCs. During spermatogenesis, germ cells are provided with suitable metabolic substrates, in a set of events mediated by SCs. Multiple signaling cascades regulate SC function and several of these signaling pathways are hormone-dependent and cell-specific. Within the seminiferous tubules, only SCs possess receptors for some hormones rendering them major targets for the hormonal signaling that regulates spermatogenesis. Although the mechanisms by which SCs fulfill their own and germ cells metabolic needs are mostly studied in vitro, SC metabolism is unquestionably a regulation point for germ cell development and the hormonal control of these processes is required for a normal spermatogenesis.     

The LRRK2 G2019S mutant exacerbates basal autophagy through activation of the MEK/ERK pathway

Mutations in leucine-rich repeat kinase 2 (LRRK2) are a major cause of familial Parkinsonism, and the G2019S mutation of LRRK2 is one of the most prevalent mutations. The deregulation of autophagic processes in nerve cells is thought to be a possible cause of Parkinson’s disease (PD). In this study, we observed that G2019S mutant fibroblasts exhibited higher autophagic activity levels than control fibroblasts. Elevated levels of autophagic activity can trigger cell death, and in our study, G2019S mutant cells exhibited increased apoptosis hallmarks compared to control cells. LRRK2 is able to induce the phosphorylation of MAPK/ERK kinases (MEK). The use of 1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene (U0126), a highly selective inhibitor of MEK1/2, reduced the enhanced autophagy and sensibility observed in G2019S LRRK2 mutation cells. These data suggest that the G2019S mutation induces autophagy via MEK/ERK pathway and that the inhibition of this exacerbated autophagy reduces the sensitivity observed in G2019S mutant cells.     

Asymmetric cell division of stem and progenitor cells during homeostasis and cancer

Stem and progenitor cells are characterized by their ability to self-renew and produce differentiated progeny. A fine balance between these processes is achieved through controlled asymmetric divisions and is necessary to generate cellular diversity during development and to maintain adult tissue homeostasis. Disruption of this balance may result in premature depletion of the stem/progenitor cell pool, or abnormal growth. In many tissues, including the brain, dysregulated asymmetric divisions are associated with cancer. Whether there is a causal relationship between asymmetric cell division defects and cancer initiation is as yet not known. Here, we review the cellular and molecular mechanisms that regulate asymmetric cell divisions in the neural lineage and discuss the potential connections between this regulatory machinery and cancer.