Formation of lentoids from retina gliocytes: ultrastructural study

In primary monolayer cultures of dispersed neural retina cells from 13-day chick embryo, gliocytes (Müller glia cells) multiply and rapidly change into a lentoidal (lens-like) phenotype. They express lens proteins, including MP26 (a lens plasma-membrane antigen) and ultra-structurally appear to resemble lens cells. A significant aspect of this modification is that the glia-derived lentoidal cells no longer display contact-affinity for neurons but become preferentially adhesive to each other; in aggregates, they assemble into compact lentoids. A likely explanation for this change in cell affinities is that the modified gliocytes express little or no R-cognin, a retinal cell-surface antigen implicated in mutual recognition and adhesion of retina cells. Although lentoidal cells express MP26, a gap-junction component in the lens, no gap junctions could be found in the lentoids.     

Arabidopsis leaf hydraulic conductance is regulated by xylem sap pH,controlled, in turn,by a P-type H+-ATPase of vascular bundle sheath cells

The leaf vascular bundle sheath cells (BSCs) that tightly envelop the leaf veins, are a selective and dynamic barrier to xylem sap water and solutes radially entering the mesophyll cells. Under normal conditions, xylem sap pH below 6 is presumably important for driving and regulating the transmembranal solute transport. Having discovered recently a differentially high expression of a BSC proton pump, AHA2, we now test the hypothesis that it regulates the xylem sap pH and leaf radial water fluxes. We monitored the xylem sap pH in the veins of detached leaves of wild-type Arabidopsis, AHA mutants and aha2 mutants complemented with AHA2 gene solely in BSCs. We tested an AHA inhibitor (vanadate) and stimulator (fusicoccin), and different pH buffers. We monitored their impact on the xylem sap pH and the leaf hydraulic conductance (K_leaf), and the effect of pH on the water osmotic permeability (P_f) of isolated BSCs protoplasts. We found that AHA2 is necessary for xylem sap acidification, and in turn, for elevating K_leaf. Conversely, AHA2 knockdown, which alkalinized the xylem sap, or, buffering its pH to 7.5, reduced K_leaf, and elevating external pH to 7.5 decreased the BSCs P_f. All these showed a causative link between AHA2 activity in BSCs and leaf radial hydraulic water conductance.     

CloneSeq: A highly sensitive analysis platform for the characterization of 3D-cultured single-cell-derived clones

1. Download : Download high-res image (151KB)
2. Download : Download full-size image

     

Notes on an interspecific interaction between distant taxa: Observation of active cohabitation and communal nesting resources between Gehyra mutilata (Wiegmann, 1834) and two vespid wasp species

Tropical ecosystems are biodiverse and ecologically complex, supporting nearly half of the global herpetofauna. Ecological interactions play a role in the maintenance of species diversity with a range of ecological interactions occurring within and among species in tropical ecosystems. Incidental observations of ecological interactions provide an important contribution to the understanding of the ecology and natural history of species. Here, we report an interspecific interaction between distant taxa, the Four-Clawed Gecko (Gehyra mutilata) utilizing an active communal nesting site and shared nesting resources with two vespid wasp species (Eumeninae and Polistinae), where previous observations documented species utilizing abandoned nesting resources. This is the first known record of three species actively cohabitating in a shared nesting resource. This observation, with one or all species positively benefiting from the ecological interaction, likely indicates a mutualistic or commensal ecological interaction. Incidental observations such as the present study are likely to reveal that interspecific ecological interactions including communal nesting are more widespread than previously thought and the co-utilization of existing nesting resources presents an advantage for taxa. Observations such as these provide the basis for understanding the complex network of ecological interactions occurring in tropical rainforests.     

The DAP-kinase interactome

DAP-kinase (DAPK) is a Ca²⁺/calmodulin regulated Ser/Thr kinase that activates a diverse range of cellular activities. It is subject to multiple layers of regulation involving both intramolecular signaling, and interactions with additional proteins, including other kinases and phosphatases. Its protein stability is modulated by at least three distinct ubiquitin-dependent systems. Like many kinases, DAPK participates in several signaling cascades, by phosphorylating additional kinases such as ZIP-kinase and protein kinase D (PKD), or Pin1, a phospho-directed peptidyl-prolyl isomerase that regulates the function of many phosphorylated proteins. Other substrate targets have more direct cellular effects; for example, phosphorylation of the myosin II regulatory chain and tropomyosin mediate some of DAPK’s cytoskeletal functions, including membrane blebbing during cell death and cell motility. DAPK induces distinct death pathways of apoptosis, autophagy and programmed necrosis. Among the substrates implicated in these processes, phosphorylation of PKD, Beclin 1, and the NMDA receptor has been reported. Interestingly, not all cellular effects are mediated by DAPK’s catalytic activity. For example, by virtue of protein–protein interactions alone, DAPK activates pyruvate kinase isoform M2, the microtubule affinity regulating kinases and inflammasome protein NLRP3, to promote glycolysis, influence microtubule dynamics, and enhance interleukin-1β production, respectively. In addition, a number of other substrates and interacting proteins have been identified, the physiological significance of which has not yet been established. All of these substrates, effectors and regulators together comprise the DAPK interactome. By presenting the components of the interactome network, this review will clarify both the mechanisms by which DAPK function is regulated, and by which it mediates its various cellular effects.     

Quantitative Models of the Dose-Response and Time Course of Inhalational Anthrax in Humans

Anthrax poses a community health risk due to accidental or intentional aerosol release. Reliable quantitative dose-response analyses are required to estimate the magnitude and timeline of potential consequences and the effect of public health intervention strategies under specific scenarios. Analyses of available data from exposures and infections of humans and non-human primates are often contradictory. We review existing quantitative inhalational anthrax dose-response models in light of criteria we propose for a model to be useful and defensible. To satisfy these criteria, we extend an existing mechanistic competing-risks model to create a novel Exposure–Infection–Symptomatic illness–Death (EISD) model and use experimental non-human primate data and human epidemiological data to optimize parameter values. The best fit to these data leads to estimates of a dose leading to infection in 50% of susceptible humans (ID₅₀) of 11,000 spores (95% confidence interval 7,200–17,000), ID₁₀ of 1,700 (1,100–2,600), and ID₁ of 160 (100–250). These estimates suggest that use of a threshold to human infection of 600 spores (as suggested in the literature) underestimates the infectivity of low doses, while an existing estimate of a 1% infection rate for a single spore overestimates low dose infectivity. We estimate the median time from exposure to onset of symptoms (incubation period) among untreated cases to be 9.9 days (7.7–13.1) for exposure to ID₅₀, 11.8 days (9.5–15.0) for ID₁₀, and 12.1 days (9.9–15.3) for ID₁. Our model is the first to provide incubation period estimates that are independently consistent with data from the largest known human outbreak. This model refines previous estimates of the distribution of early onset cases after a release and provides support for the recommended 60-day course of prophylactic antibiotic treatment for individuals exposed to low doses.