Integrating the statistical analysis of spatial data in ecology

In many areas of ecology there is an increasing emphasis on spatial relationships. Often ecologists are interested in new ways of analyzing data with the objective of quantifying spatial patterns, and in designing surveys and experiments in light of the recognition that there may be underlying spatial pattern in biotic responses. In doing so, ecologists have adopted a number of widely different techniques and approaches derived from different schools of thought, and from other scientific disciplines. While the adaptation of a diverse array of statistical approaches and methodologies for the analysis of spatial data has yielded considerable insight into various ecological problems, this diversity of approaches has sometimes impeded communication and retarded more rapid progress in this emergent area. Many of these different statistical methods provide similar information about spatial characteristics, but the differences among these methods make it difficult to compare the results of studies that employ contrasting approaches. The papers in this mini-series explore possible areas of agreement and synthesis between a diversity of approaches to spatial analysis in ecology.     

Correlation between the bone mass of athletes and biochemical and genetic markers of bone tissue remodeling

The association of the polymorphism of the VDR, Col1a1, and CALCR genes with a form of osteoporosis frequently occurring as a consequence of intense physical exercise in athletes was studied. Biochemical parameters of bone remodeling and its neuroendocrine regulation, as well as the bone masses, of 22 amateur athletes were determined immediately before a strenuous nine-week training cycle (TC) and eight months later. The possible association of these factors with the polymorphism of the genes coding for bone tissue proteins was studied. Long-term intense physical training was found to be associated with a significant activation of bone tissue resorption accompanied by continued rapid synthesis. Nevertheless, and in spite of the strong activation of resorption caused by the TC, the athletes exhibited no osteoporosis (even eight months after the discontinuation of the TC); some of them, however, displayed an individual tendency to osteopenia. According to the results of genetic analysis, this was associated with the polymorphism of predisposition genes (genotype TT of the VDR gene and the functionally weakened s allele of the Col1a1 gene).     

Phosphoproteome Profiling of the Receptor Tyrosine Kinase MuSK Identifies Tyrosine Phosphorylation of Rab GTPases

Muscle-specific receptor tyrosine kinase (MuSK) agonist antibodies were developed 2 decades ago to explore the benefits of receptor activation at the neuromuscular junction. Unlike agrin, the endogenous agonist of MuSK, agonist antibodies function independently of its coreceptor low-density lipoprotein receptor–related protein 4 to delay the onset of muscle denervation in mouse models of ALS. Here, we performed dose–response and time-course experiments on myotubes to systematically compare site-specific phosphorylation downstream of each agonist. Remarkably, both agonists elicited similar intracellular responses at known and newly identified MuSK signaling components. Among these was inducible tyrosine phosphorylation of multiple Rab GTPases that was blocked by MuSK inhibition. Importantly, mutation of this site in Rab10 disrupts association with its effector proteins, molecule interacting with CasL 1/3. Together, these data provide in-depth characterization of MuSK signaling, describe two novel MuSK inhibitors, and expose phosphorylation of Rab GTPases downstream of receptor tyrosine kinase activation in myotubes.     

Alternative splice isoforms of small conductance calcium-activated SK2 channels differ in molecular interactions and surface levels

Small conductance Ca²⁺-sensitive potassium (SK2) channels are voltage-independent, Ca²⁺-activated ion channels that conduct potassium cations and thereby modulate the intrinsic excitability and synaptic transmission of neurons and sensory hair cells. In the cochlea, SK2 channels are functionally coupled to the highly Ca²⁺ permeant α9/10-nicotinic acetylcholine receptors (nAChRs) at olivocochlear postsynaptic sites. SK2 activation leads to outer hair cell hyperpolarization and frequency-selective suppression of afferent sound transmission. These inhibitory responses are essential for normal regulation of sound sensitivity, frequency selectivity, and suppression of background noise. However, little is known about the molecular interactions of these key functional channels. Here we show that SK2 channels co-precipitate with α9/10-nAChRs and with the actin-binding protein α-actinin-1. SK2 alternative splicing, resulting in a 3 amino acid insertion in the intracellular 3′ terminus, modulates these interactions. Further, relative abundance of the SK2 splice variants changes during developmental stages of synapse maturation in both the avian cochlea and the mammalian forebrain. Using heterologous cell expression to separately study the 2 distinct isoforms, we show that the variants differ in protein interactions and surface expression levels, and that Ca²⁺ and Ca²⁺-bound calmodulin differentially regulate their protein interactions. Our findings suggest that the SK2 isoforms may be distinctly modulated by activity-induced Ca²⁺ influx. Alternative splicing of SK2 may serve as a novel mechanism to differentially regulate the maturation and function of olivocochlear and neuronal synapses.     

Genome Sequence of Staphylococcus epidermidis Strain AU12-03, Isolated from an Intravascular Catheter

In recent years, Staphylococcus epidermidis has become a major nosocomial pathogen and the most common cause of intravascular catheter-related bacteremia, which can increase morbidity and mortality and significantly affect patient recovery. We report a draft genome sequence of Staphylococcus epidermidis AU12-03, isolated from an intravascular catheter tip.     

Why cellular stress suppresses adipogenesis in skeletal tissue,but is ineffective in adipose tissue: Control of mesenchymal cell differentiation via integrin binding sites in extracellular matrices

This Perspective addresses one of the major puzzles of adipogenesis in adipose tissue, namely its resistance to cellular stress. It introduces a concept of “density” of integrin binding sites in extracellular matrix, proposes a cellular signaling explanation for the observed effects of matrix elasticity and of cell shape on mesenchymal stem cell differentiation, and discusses how specialized integrin binding sites in collagen IV-containing matrices guard two pivotal physiological and evolutionary processes: stress-resistant adipogenesis in adipose tissues and preservation of pluripotency of mesenchymal stem-like cells in their storage niches. Finally, it proposes strategies to suppress adipogenesis in adipose tissues.