Population genetic structure, phylogeography and spawning philopatry in walleye (Stizostedion vitreum) from mitochondrial DNA control region sequences

Mitochondrial (mt) DNA control region sequences were used to test the genetic and phylogeographic structure of walleye Stizostedion vitreum populations at different geographical scales: among spawning sites, lake basins, lakes, and putative glacial refugia in the Great Lakes region. Sequencing 199 walleye revealed nucleotide substitutions and tandemly repeated sequences that varied in copy number, as well as in sequence composition, in 1200 bp of the mtDNA control region. Variable numbers of copies of an 11-bp tandem repeat showed no geographical patterning and were not used in further analyses. Substitutions in the other areas of the control region yielded 19 haplotypes, revealing phylogeographic structure and significant differences among glacial refugia, lakes, basins and some spawning sites. Differences among spawning populations were consistent with reduced gene flow, philopatry and possible natal homing. Analysis of spawning populations showed consistency of genotypic frequencies among years and between males and females, supporting philopatry in both sexes. The unglaciated plateau in southern Ohio, USA housed a very different haplotype that diverged prior to the Missouri, Mississippi and Atlantic glacial refugia types. Haplotypes from the three refugia colonized the Great Lakes after retreat of the Wisconsin glaciers, and their present distribution reflects the geography of their prior isolation and differential colonization. Populations that became associated with spawning localities appear to have diverged further due to philopatry, resulting in fine-scale phylogeographic structuring.     

Winter Survival of Wild Turkey Females in Central Minnesota

Abstract: There is interest in expanding eastern wild turkey (Meleagris gallopavo silvestris) populations north of their current range. We hypothesized that winter survival and food availability are primary determinants in setting the northern extent of wild turkey distribution. To test our hypothesis, we translocated wild turkey females north of their present range into central Minnesota, USA, and compared survival in areas with supplemental food in the form of corn food plots versus areas with no supplemental food. During 2 winters with below-average snow, winter survival was higher for females with supplemental food. In one winter with above-average snow depths, survival was extremely low even with supplemental food. Supplemental food could augment survival during mild winters if wildlife managers arrange with farmers to, annually, retain standing corn near roosting habitat, but food plots may only partially offset effects of deep snow. Managers should critically evaluate northern habitats, long-term costs of sustained feeding, and potential outcomes of concentrating animals and introducing wild animals into new ecosystems. Winter survival may delimit the northern range of wild turkeys, though annual survival rates may also be important and need further research.     

Membrane Characteristics of Bursting Pacemaker Neurones in Aplysia

The group of endogenously active molluscan neurones, classified as bursting or oscillatory pacemakers, regularly fire bursts of three to fifteen impulses separated by periods of silence associated with membrane hyperpolarizations (Fig. 1a). The abdominal ganglion of the marine mollusc Aplysia californica contains six bursting pacemakers, L2-L6 (L-group) and R15¹; these cells maintain their membrane potential oscillations in the absence of synaptic input^2,3 and spike generation⁴. They also have K⁺-dependent inhibitory postsynaptic potentials (IPSPs) which last for some seconds after single or multiple discharges in the presynaptic neurones^5–8. In the L-group these IPSPs are mixed with short-lasting Cl^?-dependent IPSPs. Although there is a different transmitter responsible for the generation of these IPSPs in R15 as opposed to those in the L-group, somewhat similar difficulties were encountered in attempts to determine the mechanism(s) underlying their generation, activation of an electrogenic Na⁺ pump having been initially implicated in both cases^5,8. Just why their duration is prolonged remains uncertain, but the voltage clamp studies of Wachtel and Wilson⁹ on the L-group have again implicated a regenerative current source.     

Silencing of EEF2K (eukaryotic elongation factor-2 kinase) reveals AMPK-ULK1-dependent autophagy in colon cancer cells

EEF2K (eukaryotic elongation factor-2 kinase), also known as Ca²⁺/calmodulin-dependent protein kinase III, functions in downregulating peptide chain elongation through inactivation of EEF2 (eukaryotic translation elongation factor 2). Currently, there is a limited amount of information on the promotion of autophagic survival by EEF2K in breast and glioblastoma cell lines. However, the precise role of EEF2K in carcinogenesis as well as the underlying mechanism involved is still poorly understood. In this study, contrary to the reported autophagy-promoting activity of EEF2K in certain cancer cells, EEF2K is shown to negatively regulate autophagy in human colon cancer cells as indicated by the increase of LC3-II levels, the accumulation of LC3 dots per cell, and the promotion of autophagic flux in EEF2K knockdown cells. EEF2K negatively regulates cell viability, clonogenicity, cell proliferation, and cell size in colon cancer cells. Autophagy induced by EEF2K silencing promotes cell survival and does not potentiate the anticancer efficacy of the AKT inhibitor MK-2206. In addition, autophagy induced by silencing of EEF2K is attributed to induction of protein synthesis and activation of the AMPK-ULK1 pathway, independent of the suppression of MTOR activity and ROS generation. Knockdown of AMPK or ULK1 significantly abrogates EEF2K silencing-induced increase of LC3-II levels, accumulation of LC3 dots per cell as well as cell proliferation in colon cancer cells. In conclusion, silencing of EEF2K promotes autophagic survival via activation of the AMPK-ULK1 pathway in colon cancer cells. This finding suggests that upregulation of EEF2K activity may constitute a novel approach for the treatment of human colon cancer.