Mothering during early development influences subsequent emotional and social behaviour in Japanese quail

The aim of the present study was to investigate the influence of mothers on the emotional reactivity and social behaviour in young precocial Japanese quail. We used a classical method of maternal deprivation. Ethological tests and observations analysed and compared the behaviour of young artificially raised quail to that of young raised by adoptive maternal quail. After separation from mothers, brooded young were more fearful (frightened easily) in the presence of humans (human-observer tests) and more neophobic in novel environments (open-field and hole-in-the-wall tests) than young raised artificially. As chicks rarely expressed fear during the brooding period, no differences related to mothering could be observed at that time. In separation tests, brooded chicks jumped significantly more frequently than non-brooded chicks and later, observations of groups revealed that brooded chicks remained closer to one another than non-brooded chicks. Social motivation of brooded chicks appeared to be higher. These results indicate that, during their first days of life, mothers influence the emotional and social behaviour of their young.     

Critical role of the N-terminal residues of listeriolysin O in phagosomal escape and virulence of Listeria monocytogenes

A putative PEST sequence was recently identified close to the N-terminus of listeriolysin O (LLO), a major virulence factor secreted by the pathogenic Listeria monocytogenes. The deletion of this motif did not affect the secretion and haemolytic activity of LLO, but abolished bacterial virulence. Here, we first tested whether the replacement of the PEST motif of LLO by two different sequences, with either a very high or no PEST score, would affect phagosomal escape, protein stability and, ultimately, the virulence of L. monocytogenes. Then, we constructed LLO mutants with an intact PEST sequence but carrying mutations on either side, or on both sides, of the PEST motif. The properties of these mutants prompted us to construct three LLO mutants carrying single amino acid substitutions in the distal portion of the PEST region (P49A, K50A and P52A; preprotein numbering). Our data demonstrate that the susceptibility of LLO to intracellular proteolytic degradation is not related to the presence of a high PEST score sequence and that the insertion of two residues immediately downstream of the intact PEST sequence is sufficient to impair phagosomal escape and abolish bacterial virulence. Furthermore, we show that single amino acid substitutions in the distal portion of the PEST motif are sufficient to attenuate bacterial -virulence significantly, unravelling the critical role of this region of LLO in the pathogenesis of L. -monocytogenes.     

Woodchuck Hepatitis Virus Enhancer I and Enhancer II Are Both Involved in N-myc2 Activation in Woodchuck Liver Tumors

Direct activation of the N-myc2 oncogene by insertion of woodchuck hepatitis virus (WHV) DNA is a major oncogenic step in woodchuck hepatocarcinogenesis. We previously reported that WHV enhancer II (We2), which controls expression of the core/pregenome RNA, can also activate the N-myc2 promoter in hepatoma cell lines. To better define the integrated WHV regulatory sequences responsible for N-myc2 promoter activation in woodchuck liver tumors, we analyzed the structure and enhancer activity of a single viral integrant found at the win locus in tumor 2260T1 and mapping approximately 175 kb 3′ of N-myc2. This viral insert was made of 11 concatemerized WHV fragments, 5 of which overlapped with We2 sequences and 1 with WHV sequence homologous to that of hepatitis B virus enhancer I (We1). In transient transfection assays in hepatoma-derived cells, the We2 activator was found to be fully effective only when inserted in close proximity to the N-myc2 promoter whereas the We1 element by itself was apparently devoid of activity. In contrast, the 2260T1 viral insert exhibited a potent enhancer capacity that depended both on multimerized We2 and on We1 sequences. In a survey of different woodchuck hepatomas, both elements were commonly found within integrated viral sequences involved in long-range N-myc2 activation.     

The APPswe/PS1A246E mutations in an astrocytic cell line leads to increased vulnerability to oxygen and glucose deprivation,Ca2+ dysregulation,and mitochondrial abnormalities

Growing evidence suggests a close relationship between Alzheimer′s Disease (AD ) and cerebral hypoxia. Astrocytes play a key role in brain homeostasis and disease states, while some of the earliest changes in AD occur in astrocytes. We have therefore investigated whether mutations associated with AD increase astrocyte vulnerability to ischemia. Two astroglioma cell lines derived from APP_SWE /PS 1A246E (APP , amyloid precursor protein; PS 1, presenilin 1) transgenic mice and controls from normal mice were subjected to oxygen and glucose deprivation (OGD ), an in vitro model of ischemia. Cell death was increased in the APP_SWE /PS 1A246E line compared to the control. Increasing extracellular calcium concentration ([Ca²⁺]) exacerbated cell death in the mutant but not in the control cells. In order to explore cellular Ca²⁺ homeostasis, the cells were challenged with ATP or thapsigargin and [Ca²⁺] was measured by fluorescence microscopy. Changes in cytosolic Ca²⁺ concentration ([Ca²⁺]_c) were potentiated in the APP_SWE /PS 1A246E transgenic line. Mitochondrial function was also altered in the APP_SWE /PS 1A246E astroglioma cells; mitochondrial membrane potential and production of reactive oxygen species were increased, while mitochondrial basal respiratory rate and ATP production were decreased compared to control astroglioma cells. These results suggest that AD mutations in astrocytes make them more sensitive to ischemia; Ca²⁺ dysregulation and mitochondrial dysfunction may contribute to this increased vulnerability. Our results also highlight the role of astrocyte dyshomeostasis in the pathophysiology of neurodegenerative brain disorders.

     

Daily laying time in free-living European starlings: solar noon, a potential synchronizer

Reproduction is generally controlled by important temporal constraints involving complex adaptive mechanisms. Birds, in temperate zones, present marked breeding seasonality as well as marked daily organization of reproductive behavior, especially laying. Intra-specific variability and determinants of this pattern have been investigated mainly in domestic non-passerine birds. The present study analyzed the daily temporal organization of laying in a free-living species, the European starling, Sturnus vulgaris. Breeding in a starling colony was monitored for five consecutive years using a non-invasive method (infrared video camera) to precisely estimate laying times. European starlings present a marked daily laying rhythm, ovipositions occurring only during a morning species-specific temporal window. Inside this laying window, time intervals between successive eggs varied greatly among females. Contrary to many species, the light/dark cycle did not appear to control laying time in European starlings, but daily variations of the ultraviolet composition of the solar spectrum appeared to be a possible Zeitgeber of this behavior.     

Sliding MinPD: building evolutionary networks of serial samples via an automated recombination detection approach

MOTIVATION: Traditional phylogenetic methods assume tree-like evolutionary models and are likely to perform poorly when provided with sequence data from fast-evolving, recombining viruses. Furthermore, these methods assume that all the sequence data are from contemporaneous taxa, which is not valid for serially-sampled data. A more general approach is proposed here, referred to as the Sliding MinPD method, that reconstructs evolutionary networks for serially-sampled sequences in the presence of recombination. RESULTS: Sliding MinPD combines distance-based phylogenetic methods with automated recombination detection based on the best-known sliding window approaches to reconstruct serial evolutionary networks. Its performance was evaluated through comprehensive simulation studies and was also applied to a set of serially-sampled HIV sequences from a single patient. The resulting network organizations reveal unique patterns of viral evolution and may help explain the emergence of disease-associated mutants and drug-resistant strains with implications for patient prognosis and treatment strategies.