Intraspecific killing among Leopards (Panthera pardus) in Iran (Mammalia: Felidae)

Intraspecific aggression is one of the most common causes of death in leopards. Here, we report four cases of intraspecific killing amongst Persian Leopards (Panthera pardus saxicolor) in Iran. A young male leopard was found on 7 June 2008 which, according to camera trap images, had been killed by an adult male over a Red Deer (Cervus elaphus) kill, with trauma to his neck in Dorfak No-Hunting Area. A young female that had been fitted with a satellite GPS collar on 6 December 2015 in Tandoureh National Park died on 29 January 2016 at a site where an Urial Sheep (Ovis orientalis) ram had been freshly killed. Necropsy results, footprints at the scene of death and camera trap footage all supported the deduction that the animal was killed by a larger female leopard at the kill site. On 13 January 2017, a young, partially eaten female leopard was found with double puncture on the side of her throat. Finally, a rehabilitated adult female fitted with a satellite GPS collar found on 19 December 2017 with a double puncture on her head with several trauma and haemorrhages on her back. These instances seem to be the first documented reports of intraspecific killing among free-ranging leopards in Asia.     

A Four-Compartment Metabolomics Analysis of the Liver,Muscle, Serum,and Urine Response to Polytrauma with Hemorrhagic Shock following Carbohydrate Prefeed

Objective

Hemorrhagic shock accompanied by injury represents a major physiologic stress. Fasted animals are often used to study hemorrhagic shock (with injury). A fasted state is not guaranteed in the general human population. The objective of this study was to determine if fed animals would exhibit a different metabolic profile in response to hemorrhagic shock with trauma when compared to fasted animals.

Methods

Proton (1H) NMR spectroscopy was used to determine concentrations of metabolites from four different compartments (liver, muscle, serum, urine) taken at defined time points throughout shock/injury and resuscitation. PLS-DA was performed and VIP lists established for baseline, shock and resuscitation (10 metabolites for each compartment at each time interval) on metabolomics data from surviving animals.

Results

Fed status prior to the occurrence of hemorrhagic shock with injury alters the metabolic course of this trauma and potentially affects mortality. The death rate for CPF animals is higher than FS animals (47 vs 28%). The majority of deaths occur post-resuscitation suggesting reperfusion injury. The metabolomics response to shock reflects priorities evident at baseline. FS animals raise the baseline degree of proteolysis to provide additional amino acids for energy production while CPF animals rely on both glucose and, to a lesser extent, amino acids. During early resuscitation levels of metabolites associated with energy production drop, suggesting diminished demand.

Conclusions

Feeding status prior to the occurrence of hemorrhagic shock with injury alters the metabolic course of this trauma and potentially affects mortality. The response to shock reflects metabolic priorities at baseline.     

FlgN Is Required for Flagellum-Based Motility by Bacillus subtilis

The assembly of the bacterial flagellum is exquisitely controlled. Flagellar biosynthesis is underpinned by a specialized type III secretion system that allows export of proteins from the cytoplasm to the nascent structure. Bacillus subtilis regulates flagellar assembly using both conserved and species-specific mechanisms. Here, we show that YvyG is essential for flagellar filament assembly. We define YvyG as an orthologue of the Salmonella enterica serovar Typhimurium type III secretion system chaperone, FlgN, which is required for the export of the hook-filament junction proteins, FlgK and FlgL. Deletion of flgN (yvyG) results in a nonmotile phenotype that is attributable to a decrease in hag translation and a complete lack of filament polymerization. Analyses indicate that a flgK-flgL double mutant strain phenocopies deletion of flgN and that overexpression of flgK-flgL cannot complement the motility defect of a ΔflgN strain. Furthermore, in contrast to previous work suggesting that phosphorylation of FlgN alters its subcellular localization, we show that mutation of the identified tyrosine and arginine FlgN phosphorylation sites has no effect on motility. These data emphasize that flagellar biosynthesis is differentially regulated in B. subtilis from classically studied Gram-negative flagellar systems and questions the biological relevance of some posttranslational modifications identified by global proteomic approaches.     

Rab27a controls HIV-1 assembly by regulating plasma membrane levels of phosphatidylinositol 4,5-bisphosphate

During the late stages of the HIV-1 replication cycle, the viral polyprotein Pr55^Gag is recruited to the plasma membrane (PM), where it binds phosphatidylinositol 4,5-bisphosphate (PI(4,5)P₂) and directs HIV-1 assembly. We show that Rab27a controls the trafficking of late endosomes carrying phosphatidylinositol 4-kinase type 2 α (PI4KIIα) toward the PM of CD4⁺ T cells. Hence, Rab27a promotes high levels of PM phosphatidylinositol 4-phosphate and the localized production of PI(4,5)P₂, therefore controlling Pr55^Gag membrane association. Rab27a also controls PI(4,5)P₂ levels at the virus-containing compartments of macrophages. By screening Rab27a effectors, we identified that Slp2a, Slp3, and Slac2b are required for the association of Pr55^Gag with the PM and that Slp2a cooperates with Rab27a in the recruitment of PI4KIIα to the PM. We conclude that by directing the trafficking of PI4KIIα-positive endosomes toward the PM, Rab27a controls PI(4,5)P₂ production and, consequently, HIV-1 replication.     

The Drosophila innexin 7 gap junction protein is required for development of the embryonic nervous system

The Drosophila genome encodes eight members of the innexin family of gap junction proteins. Most of the family members are expressed in complex and overlapping expression patterns during Drosophila development. Functional studies and mutant analysis have been performed for only few of the innexin genes. The authors generated an antibody against Innexin7 and studied its expression and functional role in embryonic development by using transgenic RNA interference (RNAi) lines. The authors found Innexin7 protein expression in all embryonic epithelia from early to late stages of development, including in the developing epidermis and the gastrointestinal tract. In early embryonic stages, the authors observed a nuclear localization of Innexin7, whereas Innexin7 was found in a punctuate pattern in the cytoplasm and at the membrane of most epithelial tissues at later stages of development. During central nervous system (CNS) development, Innexin7 was expressed in cells of the neuroectoderm and the mesectoderm and at later stages of embryogenesis, its expression was largely restricted to a segmental pattern of few glia and neuronal cells derived from the midline precursors. Coimmunostaining experiments showed that Innexin7 is expressed in midline glia, and in two different neuronal cells, the pCC and MP2 neurons, which are pioneer cells for axon guidance. RNAi-mediated knock down was used to gain insight into the embryonic function of innexin7. Down-regulation of innexin7 expression resulted in a severe disruption of embryonic nervous system development. Longitudinal, posterior, and anterior commissures were disrupted and the outgrowth of axon fibers of the ventral nerve cord was aberrant, causing peripheral nervous system defects. The results suggest an essential role for innexin7 for axon guidance and embryonic nervous system development in Drosophila.