Tree Species Traits but Not Diversity Mitigate Stem Breakage in a Subtropical Forest following a Rare and Extreme Ice Storm

Future climates are likely to include extreme events, which in turn have great impacts on ecological systems. In this study, we investigated possible effects that could mitigate stem breakage caused by a rare and extreme ice storm in a Chinese subtropical forest across a gradient of forest diversity. We used Bayesian modeling to correct stem breakage for tree size and variance components analysis to quantify the influence of taxon, leaf and wood functional traits, and stand level properties on the probability of stem breakage. We show that the taxon explained four times more variance in individual stem breakage than did stand level properties; trees with higher specific leaf area (SLA) were less susceptible to breakage. However, a large part of the variation at the taxon scale remained unexplained, implying that unmeasured or undefined traits could be used to predict damage caused by ice storms. When aggregated at the plot level, functional diversity and wood density increased after the ice storm. We suggest that for the adaption of forest management to climate change, much can still be learned from looking at functional traits at the taxon level.     

High count rates with total internal reflection fluorescence correlation spectroscopy

We have modeled the structure of KirBac1.1 in an open state using as a starting point the structure of KirBac1.1 in its closed conformation (Protein Data Bank 1P7B). To test the validity of the open-state model, molecular dynamics simulations in octane, a lipid bilayer mimetic, were carried out. Simulations of the closed conformer were used for comparison purposes. The total simulation time was approximately 138 ns. The initial open model was refined by using projection maps obtained from electron microscopy experiments on two-dimensional crystals of the inwardly rectifying K+ channel KirBac3.1 from Magentospirillum magnetotacticum captured in its open state (C. Vénien-Bryan, unpublished data). Significant movements of the outer helices take place in going from the closed to the open model in agreement with structural and biochemical data in potassium channels, which suggests that gating is accomplished by a conformational change that takes place in the transmembrane domain upon an external stimulus. The motion of the inner helices is mainly achieved by bending at conserved glycine residues that have been previously reported to act as molecular hinges. Overall, these simulations suggest that the open conformer is stable, providing a plausible all-atom model that will enable the study of potential gating mechanisms in more detail.     

Linkage data suggesting allelic heterogeneity for paramyotonia congenita and hyperkalemic periodic paralysis on chromosome 17

Summary Paramyotonia congenita (PC), an autosomal dominant non-progressive muscle disorder, is characterised by cold-induced stiffness followed by muscle weakness. The weakness is caused by a dysfunction of the sodium channel in muscle fibre. Parts of the gene coding for the -subunit of the sodium channel of the adult human skeletal muscle (SCN4A) have been localised on chromosome 17. To investigate the role of this gene in the etiology of PC, a linkage analysis in 17 well-defined families was carried out. The results (z=20.61, =0.001) show that the mutant gene responsible for the disorder is indeed tightly linked to the SCN4A gene. The mutation causing hyperkalemic periodic paralysis (HyperPP) with myotonia has previously been mapped to this gene locus by the same candidate gene approach. Thus, our data suggest that PC and HyperPP are caused by allelic mutations at a single locus on chromosome 17.Dedicated to Professor P. E. Becker on the occasion of his 83rd birthday.     

No evidence for linkage of autosomal dominant proximal spinal muscular atrophies to chromosome 5q markers

Summary Two recent articles have reported the linkage of a gene for recessive spinal muscular atrophy (SMA) on the chromosome region 5q11.2–13.3. Our data show no linkage of the dominantly inherited forms of SMA to this chromosome region.     

Can amphibians take the heat? Vulnerability to climate warming in subtropical and temperate larval amphibian communities

Predicting the biodiversity impacts of global warming implies that we know where and with what magnitude these impacts will be encountered. Amphibians are currently the most threatened vertebrates, mainly due to habitat loss and to emerging infectious diseases. Global warming may further exacerbate their decline in the near future, although the impact might vary geographically. We predicted that subtropical amphibians should be relatively susceptible to warming‐induced extinctions because their upper critical thermal limits (CT_max) might be only slightly higher than maximum pond temperatures (T_max). We tested this prediction by measuring CT_max and T_max for 47 larval amphibian species from two thermally distinct subtropical communities (the warm community of the Gran Chaco and the cool community of Atlantic Forest, northern Argentina), as well as from one European temperate community. Upper thermal tolerances of tadpoles were positively correlated (controlling for phylogeny) with maximum pond temperatures, although the slope was steeper in subtropical than in temperate species. CT_max values were lowest in temperate species and highest in the subtropical warm community, which paradoxically, had very low warming tolerance (CT_max–T_max) and therefore may be prone to future local extinction from acute thermal stress if rising pond T_max soon exceeds their CT_max. Canopy‐protected subtropical cool species have larger warming tolerance and thus should be less impacted by peak temperatures. Temperate species are relatively secure to warming impacts, except for late breeders with low thermal tolerance, which may be exposed to physiological thermal stress in the coming years.     

Genomic deletion and promoter methylation status of Hypermethylated in Cancer 1 (HIC1) in mantle cell lymphoma

Mantle cell lymphomas (MCL), characterized by the t(11;14)(q13;q32), frequently carry secondary genetic alterations such as deletions in chromosome 17p involving the TP53 locus. Given that the association between TP53-deletions and concurrent mutations of the remaining allele is weak and based on our recent report that the Hypermethylated in Cancer 1 (HIC1) gene, that is located telomeric to the TP53 gene, may be targeted by deletions in 17p in diffuse large B-cell lymphoma (DLBCL), we investigated whether HIC1 inactivations might also occur in MCL. Monoallelic deletions of the TP53 locus were detected in 18 out of 59 MCL (31%), while overexpression of p53 protein occurred in only 8 out of 18 of these MCL (44%). In TP53-deleted MCL, the HIC1 gene locus was co-deleted in 11 out of 18 cases (61%). However, neither TP53 nor HIC1 deletions did affect survival of MCL patients. In most analyzed cases, no hypermethylation of the HIC1 exon 1A promoter was observed (17 out of 20, 85%). However, in MCL cell lines without HIC1-hypermethylation, the mRNA expression levels of HIC1 were nevertheless significantly reduced, when compared to reactive lymph node specimens, pointing to the occurrence of mechanisms other than epigenetic or genetic events for the inactivation of HIC1 in this entity.