University Of Lie Ge

Gembloux, Belgium

University Of Lie Ge

Gembloux, Belgium
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Vleminckx J.,Free University of Colombia | Morin-Rivat J.,University Of Lie Ge | Morin-Rivat J.,Royal Museum for Central Africa | Biwole A.B.,University Of Lie Ge | And 6 more authors.
PLoS ONE | Year: 2014

The canopy of many central African forests is dominated by light-demanding tree species that do not regenerate well under themselves. The prevalence of these species might result from ancient slash-and-burn agricultural activities that created large openings, while a decline of these activities since the colonial period could explain their deficit of regeneration. To verify this hypothesis, we compared soil charcoal abundance, used as a proxy for past slash-and-burn agriculture, and tree species composition assessed on 208 rainforest 0.2 ha plots located in three areas from Southern Cameroon. Species were classified in regeneration guilds (pioneer, non-pioneer light-demanding, shade-bearer) and characterized by their woodspecific gravity, assumed to reflect light requirement. We tested the correlation between soil charcoal abundance and: (i) the relative abundance of each guild, (ii) each species and family abundance and (iii) mean wood-specific gravity. Charcoal was found in 83% of the plots, indicating frequent past forest fires. Radiocarbon dating revealed two periods of fires: ''recent'' charcoal were on average 300 years old (up to 860 BP, n = 16) and occurred in the uppermost 20 cm soil layer, while ''ancient'' charcoal were on average 1900 years old (range: 1500 to 2800 BP, n = 43, excluding one sample dated 9400 BP), and found in all soil layers. While we expected a positive correlation between the relative abundance of lightdemanding species and charcoal abundance in the upper soil layer, overall there was no evidence that the current heterogeneity in tree species composition can be explained by charcoal abundance in any soil layer. The absence of signal supporting our hypothesis might result from (i) a relatively uniform impact of past slash-and-burn activities, (ii) pedoturbation processes bringing ancient charcoal to the upper soil layer, blurring the signal of centuries-old Human disturbances, or (iii) the prevalence of other environmental factors on species composition. © 2014 Vleminckx et al.

Avila A.,Hasselt University | Avila A.,University of Liège | Avila A.,University of Lie Ge | Vidal P.M.,Hasselt University | And 11 more authors.
Cell Death and Differentiation | Year: 2014

The development of the cerebral cortex requires coordinated regulation of proliferation, specification, migration and differentiation of cortical progenitors into functionally integrated neurons. The completion of the neurogenic program requires a dynamic interplay between cell intrinsic regulators and extrinsic cues, such as growth factor and neurotransmitters. We previously demonstrated a role for extrasynaptic glycine receptors (GlyRs) containing the α2 subunit in cerebral cortical neurogenesis, revealing that endogenous GlyR activation promotes interneuron migration in the developing cortical wall. The proliferative compartment of the cortex comprises apical progenitors that give birth to neurons directly or indirectly through the generation of basal progenitors, which serve as amplification step to generate the bulk of cortical neurons. The present work shows that genetic inactivation of Glra2, the gene coding the α2 subunit of GlyRs, disrupts dorsal cortical progenitor homeostasis with an impaired capability of apical progenitors to generate basal progenitors. This defect results in an overall reduction of projection neurons that settle in upper or deep layers of the cerebral cortex. Overall, the depletion of cortical neurons observed in Glra2-knockout embryos leads to moderate microcephaly in newborn Glra2-knockout mice. Taken together, our findings support a contribution of GlyR α2 to early processes in cerebral cortical neurogenesis that are required later for the proper development of cortical circuits. © 2015 Macmillan Publishers Limited.

Vanhaudenhuyse A.,University of Lie Ge | Noirhomme Q.,University of Lie Ge | Tshibanda L.J.-F.,University of Lie Ge | Tshibanda L.J.-F.,University of Liège | And 16 more authors.
Brain | Year: 2010

The 'default network' is defined as a set of areas, encompassing posterior-cingulate/precuneus, anterior cingulate/mesiofrontal cortex and temporo-parietal junctions, that show more activity at rest than during attention-demanding tasks. Recent studies have shown that it is possible to reliably identify this network in the absence of any task, by resting state functional magnetic resonance imaging connectivity analyses in healthy volunteers. However, the functional significance of these spontaneous brain activity fluctuations remains unclear. The aim of this study was to test if the integrity of this resting-state connectivity pattern in the default network would differ in different pathological alterations of consciousness. Fourteen non-communicative brain-damaged patients and 14 healthy controls participated in the study. Connectivity was investigated using probabilistic independent component analysis, and an automated template-matching component selection approach. Connectivity in all default network areas was found to be negatively correlated with the degree of clinical consciousness impairment, ranging from healthy controls and locked-in syndrome to minimally conscious, vegetative then coma patients. Furthermore, precuneus connectivity was found to be significantly stronger in minimally conscious patients as compared with unconscious patients. Locked-in syndrome patient's default network connectivity was not significantly different from controls. Our results show that default network connectivity is decreased in severely brain-damaged patients, in proportion to their degree of consciousness impairment. Future prospective studies in a larger patient population are needed in order to evaluate the prognostic value of the presented methodology.

Vanhee C.,Catholic University of Louvain | Guillon S.,Catholic University of Louvain | Masquelier D.,Catholic University of Louvain | Degand H.,Catholic University of Louvain | And 3 more authors.
Journal of Experimental Botany | Year: 2011

AtTSPO is a TspO/MBR domain-protein potentially involved in multiple stress regulation in Arabidopsis. As in most angiosperms, AtTSPO is encoded by a single, intronless gene. Expression of AtTSPO is tightly regulated both at the transcriptional and post-translational levels. It has been shown previously that overexpression of AtTSPO in plant cell can be detrimental, and the protein was detected in the endoplasmic reticulum (ER) and Golgi stacks, contrasting with previous findings and suggesting a mitochondrial subcellular localization for this protein. To ascertain these findings, immunocytochemistry and ABA induction were used to demonstrate that, in plant cells, physiological levels of AtTSPO colocalized with AtArf1, a mainly Golgi-localized protein in plant cells. In addition, fluorescent protein-tagged AtTSPO was targeted to the secretory pathway and did not colocalize with MitoTracker-labelled mitochondria. These results suggest that the polytopic membrane protein AtTSPO is cotranslationally targeted to the ER in plant cells and accumulates in the Trans-Golgi Network. Heterologous expression of AtTSPO in Saccharomyces cerevisiae, yeast devoid of TSPO-related protein, resulted in growth defects. However, subcellular fractionation and immunoprecipitation experiments showed that AtTSPO was targeted to mitochondria where it colocalized and interacted with the outer mitochondrial membrane porin VDAC1p, reminiscent of the subcellular localization and activity of mammalian translocator protein 18 kDa TSPO. The evolutionarily divergent AtTSPO appears therefore to be switching its sorting mode in a species-dependent manner, an uncommon peculiarity for a polytopic membrane protein in eukaryotic cells. These results are discussed in relation to the recognition and organelle targeting mechanisms of polytopic membrane proteins in eukaryotic cells. © 2010 The Author(s).

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