Description de Falklandia gen.n. de I'Ocean Austral et définition des Lysianassoidea uristidiens (Crustacea, Amphipoda)

The revision of the antarctic–subantarctic species Orchomenopsis reducta Schellenberg, 1931, has led to its attribution to a new, highly apomorphic genus: Falklandia gen.n. A new definition of the uristid group is given and Falklandia with 36 other lysianassoid genera are attributed to this supposedly monophyletic group.     

Hyphal morphogenesis in Aspergillus nidulans

The formation of hyphae that grow solely by apical extension is a defining feature of filamentous fungi. Hyphal morphogenesis involves several key steps, including the establishment and maintenance of a stable polarity axis, as well as cell division via the deposition of septa. Several filamentous fungi have been employed in attempts to decipher the mechanisms underlying these steps. Amongst these fungi, Aspergillus nidulans has proven to be a particularly valuable model. The genetic tractability of this fungus coupled with the availability of sophisticated post-genomics resources has enabled the identification and characterization of numerous genes involved in hyphal morphogenesis. Here, we summarize current progress towards understanding the function of these genes and the mechanisms involved in polarized hyphal growth and septation in A. nidulans. We also highlight important areas for future investigation.     

Human P301L-Mutant Tau Expression in Mouse Entorhinal-Hippocampal Network Causes Tau Aggregation and Presynaptic Pathology but No Cognitive Deficits

Accumulation of hyperphosphorylated tau in the entorhinal cortex (EC) is one of the earliest pathological hallmarks in patients with Alzheimer’s disease (AD). It can occur before significant Aβ deposition and appears to “spread” into anatomically connected brain regions. To determine whether this early-stage pathology is sufficient to cause disease progression and cognitive decline in experimental models, we overexpressed mutant human tau (hTauP301L) predominantly in layer II/III neurons of the mouse EC. Cognitive functions remained normal in mice at 4, 8, 12 and 16 months of age, despite early and extensive tau accumulation in the EC. Perforant path (PP) axon terminals within the dentate gyrus (DG) contained abnormal conformations of tau even in young EC-hTau mice, and phosphorylated tau increased with age in both the EC and PP. In old mice, ultrastructural alterations in presynaptic terminals were observed at PP-to-granule cell synapses. Phosphorylated tau was more abundant in presynaptic than postsynaptic elements. Human and pathological tau was also detected within hippocampal neurons of this mouse model. Thus, hTauP301L accumulation predominantly in the EC and related presynaptic pathology in hippocampal circuits was not sufficient to cause robust cognitive deficits within the age range analyzed here.     

Thyroxine-induced differential mortality of cleft lip mouse embryos: dose- and time-response studies of the A/WySn strain

Pregnant A/WySn mice, 20 to 30% of whose offspring have spontaneous cleft lip, were treated with thyroxine. Following treatment, cleft lip and normal embryos died, but cleft lip embryos died at a higher rate. The increased liability of cleft lip embryos to thyroxine-induced death was considered as a possible experimental route to identify the basic genetic defect that causes cleft lip. A time-response study indicated that cleft lip embryos responded more than normals following treatment on any of days 7 to 12 of gestation, that there is no sharply defined critical period, and that normal and cleft lip embryos do not differ in time of maximum sensitivity. A dose-response study showed linear responses of normal and cleft lip embryos on a probit-log dose scale, with a common slope and LD50's of 1.9 and 1.3 mg respectively. These dose-response properties indicate that normal and cleft lip embryos are probably killed by the same mechanism, but differ in dosage tolerance. That is, they differ quantitatively, not qualitatively. Thyroxine did not significantly change the cleft lip frequency, and the difference between normal and cleft lip embryos that leads to cleft lip itself is therefore not in the same pathway as that which leads to thyroxine-induced death. A hypothetical example of the defect basic to both pathways is presented.