Effects of stimuli shape and polarization in evoking deimatic patterns in the European cuttlefish, Sepia officinalis, under varying turbidity conditions

Cuttlefish possess the complex ability to identify approaching threats and then to selectively express the appropriate defense. We examined the visual cues used by Sepia officinalis cuttlefish during predator detection and the responses they selected. Using computer-generated stimuli, we set out to quantitate the deimatic responses to artificial looming stimuli of different shapes and contrasts. Defensive behavior gradually intensified as geometrical shapes resembled an image of a fish. Therefore, in addition to an object’s size or its sudden increase in size, cuttlefish use form recognition to identify a threat. Cuttlefish demonstrated equal performance in predator detection trough clear water when presented with intensity versus polarization contrasts. However, when the water turbidity increased, the cuttlefish still detected looming fish shapes based on polarization contrast even when intensity information alone did not suffice. These results demonstrate the interplay between intensity and polarization information transmission and processing in the spatial domain. As nectobenthic organisms, cuttlefish probably experience low visibility conditions on a regular basis. The ability to see further into turbid water and to better detect an approaching object would be beneficial for their survival.     

Germline stem cell arrest inhibits the collapse of somatic proteostasis early in Caenorhabditis elegans adulthood

All cells rely on highly conserved protein folding and clearance pathways to detect and resolve protein damage and to maintain protein homeostasis (proteostasis). Because age is associated with an imbalance in proteostasis, there is a need to understand how protein folding is regulated in a multicellular organism that undergoes aging. We have observed that the ability of Caenorhabditis elegans to maintain proteostasis declines sharply following the onset of oocyte biomass production, suggesting that a restricted protein folding capacity may be linked to the onset of reproduction. To test this hypothesis, we monitored the effects of different sterile mutations on the maintenance of proteostasis in the soma of C. elegans. We found that germline stem cell (GSC) arrest rescued protein quality control, resulting in maintenance of robust proteostasis in different somatic tissues of adult animals. We further demonstrated that GSC‐dependent modulation of proteostasis requires several different signaling pathways, including hsf‐1 and daf‐16/kri‐1/tcer‐1, daf‐12, daf‐9, daf‐36, nhr‐80, and pha‐4 that differentially modulate somatic quality control functions, such that each signaling pathway affects different aspects of proteostasis and cannot functionally complement the other pathways. We propose that the effect of GSCs on the collapse of proteostasis at the transition to adulthood is due to a switch mechanism that links GSC status with maintenance of somatic proteostasis via regulation of the expression and function of different quality control machineries and cellular stress responses that progressively lead to a decline in the maintenance of proteostasis in adulthood, thereby linking reproduction to the maintenance of the soma.     

Recovering population parameters from a single gene genealogy: an unbiased estimator of the growth rate

We show that the number of lineages ancestral to a sample, as a function of time back into the past, which we call the number of lineages as a function of time (NLFT), is a nearly deterministic property of large-sample gene genealogies. We obtain analytic expressions for the NLFT for both constant-sized and exponentially growing populations. The low level of stochastic variation associated with the NLFT of a large sample suggests using the NLFT to make estimates of population parameters. Based on this, we develop a new computational method of inferring the size and growth rate of a population from a large sample of DNA sequences at a single locus. We apply our method first to a sample of 1,212 mitochondrial DNA (mtDNA) sequences from China, confirming a pattern of recent population growth previously identified using other techniques, but with much smaller confidence intervals for past population sizes due to the low variation of the NLFT. We further analyze a set of 63 mtDNA sequences from blue whales (BWs), concluding that the population grew in the past. This calls for reevaluation of previous studies that were based on the assumption that the BW population was fixed.     

Medical sequencing at the extremes of human body mass

Body weight is a quantitative trait with significant heritability in humans. To identify potential genetic contributors to this phenotype, we resequenced the coding exons and splice junctions of 58 genes in 379 obese and 378 lean individuals. Our 96-Mb survey included 21 genes associated with monogenic forms of obesity in humans or mice, as well as 37 genes that function in body weight-related pathways. We found that the monogenic obesity-associated gene group was enriched for rare nonsynonymous variants unique to the obese population compared with the lean population. In addition, computational analysis predicted a greater fraction of deleterious variants within the obese cohort. Together, these data suggest that multiple rare alleles contribute to obesity in the population and provide a medical sequencing-based approach to detect them.     

Mouse models for human deafness: current tools for new fashions

Mouse models are one of the major tools used for discovery and characterization of genes for non-syndromic deafness in humans. The similarities between the mouse and human genomes, and between the physiology and morphology of their auditory systems, are striking. This article describes the latest mouse models, including spontaneous, 'knockout' and ENU (N-ethyl-N-nitrosourea)-induced mutants, and the recent discovery of modifier genes that are involved in mouse deafness; this discovery is leading the search for genetic modifiers for human disorders.     

Electroendocytosis Is Driven by the Binding of Electrochemically Produced Protons to the Cell’s Surface

Electroendocytosis involves the exposure of cells to pulsed low electric field and is emerging as a complementary method to electroporation for the incorporation of macromolecules into cells. The present study explores the underlying mechanism of electroendocytosis and its dependence on electrochemical byproducts formed at the electrode interface. Cell suspensions were exposed to pulsed low electric field in a partitioned device where cells are spatially restricted relative to the electrodes. The cellular uptake of dextran-FITC was analyzed by flow cytometery and visualized by confocal microscopy. We first show that uptake occurs only in cells adjacent to the anode. The enhanced uptake near the anode is found to depend on electric current density rather than on electric field strength, in the range of 5 to 65 V/cm. Electrochemically produced oxidative species that impose intracellular oxidative stress, do not play any role in the stimulated uptake. An inverse dependence is found between electrically induced uptake and the solution’s buffer capacity. Electroendocytosis can be mimicked by chemically acidifying the extracellular solution which promotes the enhanced uptake of dextran polymers and the uptake of plasmid DNA. Electrochemical production of protons at the anode interface is responsible for inducing uptake of macromolecules into cells exposed to a pulsed low electric field. Expanding the understanding of the mechanism involved in electric fields induced drug-delivery into cells, is expected to contribute to clinical therapy applications in the future.