Biogeographic historical legacies in the net primary productivity of Northern Hemisphere forests

It has been suggested that biogeographic historical legacies in plant diversity may influence ecosystem functioning. This is expected because of known diversity effects on ecosystem functions, and impacts of historical events such as past climatic changes on plant diversity. However, empirical evidence for a link between biogeographic history and present‐day ecosystem functioning is still limited. Here, we explored the relationships between Late‐Quaternary climate instability, species‐pool size, local species and functional diversity, and the net primary productivity (NPP) of Northern Hemisphere forests using structural equation modelling. Our study confirms that past climate instability has negative effects on plant functional diversity and through that on NPP, after controlling for present‐day climate, soil conditions, stand biomass and age. We conclude that global models of terrestrial plant productivity need to consider the biogeographical context to improve predictions of plant productivity and feedbacks with the climate system.     

Mutations in the TGFβ binding-protein-like domain 5 of FBN1 are responsible for acromicric and geleophysic dysplasias

Geleophysic (GD) and acromicric dysplasia (AD) belong to the acromelic dysplasia group and are both characterized by severe short stature, short extremities, and stiff joints. Although AD has an unknown molecular basis, we have previously identified ADAMTSL2 mutations in a subset of GD patients. After exome sequencing in GD and AD cases, we selected fibrillin 1 (FBN1) as a candidate gene, even though mutations in this gene have been described in Marfan syndrome, which is characterized by tall stature and arachnodactyly. We identified 16 heterozygous FBN1 mutations that are all located in exons 41 and 42 and encode TGFβ-binding protein-like domain 5 (TB5) of FBN1 in 29 GD and AD cases. Microfibrillar network disorganization and enhanced TGFβ signaling were consistent features in GD and AD fibroblasts. Importantly, a direct interaction between ADAMTSL2 and FBN1 was demonstrated, suggesting a disruption of this interaction as the underlying mechanism of GD and AD phenotypes. Although enhanced TGFβ signaling caused by FBN1 mutations can trigger either Marfan syndrome or GD and AD, our findings support the fact that TB5 mutations in FBN1 are responsible for short stature phenotypes.     

Bacterial Community Composition in Lake Tanganyika: Vertical and Horizontal Heterogeneity

Vertical and latitudinal differences in bacterial community composition (BCC) in Lake Tanganyika were studied during the dry season of 2002 by means of denaturing gradient gel electrophoresis analysis of PCR-amplified 16S RNA fragments. Dominant bands were sequenced and identified as members of the Cyanobacteria, Actinobacteria, Nitrospirae, green nonsulfur bacteria, and Firmicutes divisions and the Gamma- and Deltaproteobacteria subdivisions. The BCC in the lake displayed both vertical and latitudinal variation. Vertical changes in BCC were related to the thermal water column stratification, which influences oxygen and nutrient concentrations. Latitudinal variation was related to upwelling of deep water and increased primary production in the south of the lake. The number of bands per sample increased with bacterial production in the epilimnion of the lake, suggesting a positive diversity-productivity relationship.     

The phenotypic spectrum of the 10p deletion syndrome versus the classical DiGeorge syndrome

We reviewed 36 patients with a deletion of the short arm of chromosome 10 and a partial DiGeorge syndrome. We compared the phenotypes observed in these del(10p) patients with the classical DiGeorge phenotype associated with del(22q11), pointing out both similarities and differences. Some features, such as sensorineural hearing loss, seem to be highly associated with a deletion of 10p but are absent in the classical DiGeorge spectrum caused by del(22q11).     

Fragmin60 encodes an actin-binding protein with a C2 domain and controls actin Thr-203 phosphorylation in Physarum plasmodia and sclerotia

We report the isolation of a cDNA clone encoding a 60-kDa protein termed fragmin60 that cross-reacts with fragmin antibodies. Unlike other gelsolin-related proteins, fragmin60 contains a unique N-terminal domain that shows similarity with C2 domains of aczonin, protein kinase C, and synaptotagmins. The fragmin60 C2 domain binds three calcium ions, one with nanomolar affinity and two with micromolar affinity. Actin binding by fragmin60 requires higher calcium concentrations than does binding of actin by a fragmin60 mutant lacking the C2 domain, suggesting that the C2 domain secures the actin binding moiety in a conformation preventing actin binding at low calcium concentrations. The fragmin60 C2 domain does not bind phospholipids but interacts with the endogenous homologue of Saccharomyces cerevisiae S-phase kinase-associated protein (Skp1), as shown by pull-down assays and co-expression in mammalian cells. Recombinant fragmin60 promotes in vitro phosphorylation of actin Thr-203 by the actin-fragmin kinase. We further show that in vivo phosphorylation of actin in the fragmin60-actin complex occurs in sclerotia, a dormant stage of Physarum development, as well as in plasmodia. Our findings indicate that we have cloned a novel type of gelsolin-related actin-binding protein that is involved in controlling regulation of actin phosphorylation in vivo.