The effects of starvation and sexual maturation on Na+ transbranchial fluxes following direct transfer from fresh water to sea-water in rainbow trout (Salmo gairdneri)

1. The perfused isolated head technique has been used to measure sodium arterial fluxes following direct transfer from fresh water to sea-water. 2. A starvation-related decrease in net sodium flux is reported. 3. Sexual maturation slackens the decrement of this net flux. 4. In starved fish, the cytological modifications of chloride cells following such a transfer are delayed. 5. This effect of starvation is discussed in terms of lamella sodium imperviousness.     

Alterations in Oxidative Markers in the Cerebellum and Peripheral Organs in MPS I Mice

Mucopolysaccharidosis type I is a lysosomal storage disease with alterations in several organs. Little is known about the pathways that lead to the pathology. Evidences point oxidative stress on lysosomal storage diseases and mucopolysaccharidosis type I. The aim of the present study was to evaluate oxidative biomarkers on mucopolysaccharidosis type I mice model. We evaluated antioxidant enzymatic activity, protein damage and lipid peroxidation in the forebrain, cerebellum, heart, lung, diaphragm, liver, kidney and spleen. Superoxide dismutase activity was increased on cerebellum, lung, diaphragm, liver and kidney of mucopolysaccharidosis type I mice. Catalase activity was increased on cerebellum, spleen and lung. There was no alteration on glutathione peroxidase activity on any of the analyzed organs. Mucopolysaccharidosis type I mice showed increased carbonyl groups on cerebellum, heart and spleen. There was a decrease of thiobarbituric acid-reactive substances on the cerebellum of mucopolysaccharidosis type I mice. The results indicate a oxidative imbalance in this model. As lysosomes are very susceptible to oxidative damage, leading inclusive to cellular death, and lysosomal storage diseases present several alterations on this organelles, this finding can help to elucidate the cellular damage pathways on mucopolysaccharidosis type I.     

Global phylogeography with mixed-marker analysis reveals male-mediated dispersal in the endangered scalloped hammerhead shark (Sphyrna lewini)

Background

The scalloped hammerhead shark, Sphyrna lewini, is a large endangered predator with a circumglobal distribution, observed in the open ocean but linked ontogenetically to coastal embayments for parturition and juvenile development. A previous survey of maternal (mtDNA) markers demonstrated strong genetic partitioning overall (global Φ_ST = 0.749) and significant population separations across oceans and between discontinuous continental coastlines.

Methodology/Principal Findings

We surveyed the same global range with increased sample coverage (N = 403) and 13 microsatellite loci to assess the male contribution to dispersal and population structure. Biparentally inherited microsatellites reveal low or absent genetic structure across ocean basins and global genetic differentiation (F _ST = 0.035) over an order of magnitude lower than the corresponding measures for maternal mtDNA lineages (Φ_ST = 0.749). Nuclear allelic richness and heterozygosity are high throughout the Indo-Pacific, while genetic structure is low. In contrast, allelic diversity is low while population structure is higher for populations at the ends of the range in the West Atlantic and East Pacific.

Conclusions/Significance

These data are consistent with the proposed Indo-Pacific center of origin for S. lewini, and indicate that females are philopatric or adhere to coastal habitats while males facilitate gene flow across oceanic expanses. This study includes the largest sampling effort and the most molecular loci ever used to survey the complete range of a large oceanic predator, and findings emphasize the importance of incorporating mixed-marker analysis into stock assessments of threatened and endangered shark species.     

spe-29 encodes a small predicted membrane protein required for the initiation of sperm activation in Caenorhabditis elegans

Caenorhabditis elegans spermatids complete a dramatic morphogenesis to crawling spermatozoa in the absence of an actin- or tubulin-based cytoskeleton and without synthesizing new gene products. Mutations in three genes (spe-8, spe-12, and spe-27) prevent the initiation of this morphogenesis, termed activation. Males with mutations in any of these genes are fertile. By contrast, mutant hermaphrodites are self-sterile when unmated due to a failure in spermatid activation. Intriguingly, mutant hermaphrodites form functional spermatozoa and become self-fertile upon mating, suggesting that spermatids can be activated by male seminal fluid. Here we describe a mutation in a fourth gene, spe-29, which mimics the phenotype of spe-8, spe-12, and spe-27 mutants. spe-29 sperm are defective in the initiation of hermaphrodite sperm activation, yet they maintain the ability to complete the morphogenetic rearrangements that follow. Mutant alleles of spe-12, spe-27, and spe-29 exhibit genetic interactions that suggest that the wild-type products of these genes function in a common signaling pathway to initiate sperm activation. We have identified the spe-29 gene, which is expressed specifically in the sperm-producing germ line and is predicted to encode a small, novel transmembrane protein.     

New microsatellite loci for the endangered scalloped hammerhead shark, Sphyrna lewini

We isolated 15 microsatellite markers for the scalloped hammerhead shark, Sphyrna lewini. Loci were tested on 80 specimens of S. lewini from four Eastern Pacific samples. The number of alleles per locus ranged from 6 to 31 (mean = 14). Observed and expected levels of heterozygosity per locus ranged from 0.39 to 0.91 (mean = 0.70) and from 0.54 to 0.90 (mean = 0.76), respectively. No pairs of loci were in gametic disequilibrium after Bonferroni correction of α. One locus showed significantly lower heterozygosity than expected under Hardy–Weinberg proportions in two populations, possibly caused by null alleles.     

Effect of acute adrenalectomy on sympathetic responses to peripheral lipopolysaccharide or central PGE(2)

The impact of plasma corticosterone levels on the sympathetic nervous system (SNS) response to intravenous lipopolysaccharide (LPS) or intracerebroventricular injections of PG was studied in anesthetized (urethan-chloralose) male Sprague-Dawley rats. For this, electrophysiological recordings of splenic and renal nerves were completed in control or adrenalectomized (ADX) rats. LPS (10 microgram iv) similarly increased splenic and renal nerve activity in control rats with a shorter onset latency for the splenic nerve. Acute ADX enhanced the response of both nerves to LPS (P < 0.005) and reduced the onset latency of the renal nerve (P < 0.05). PGE(2) (2 microgram icv) rapidly increased the activity of both nerves but preferentially (magnitude and onset latency) stimulated the renal nerve (P < 0.05). The magnitude of the splenic nerve response to PGE(2) was unaffected by ADX. Unexpectedly, PGE(2) was less effective at stimulating renal nerve activity in ADX animals relative to intact controls (P < 0.05). Pretreatment of ADX rats with a CRF antagonist ([D-Phe(12), Nle(21,38), Calpha-MeLeu(37)]CRF-(12-41)) reversed this effect such that the renal nerve responded to central PGE(2) to a greater extent than the splenic nerve (P < 0.05), as was the case in non-ADX rats. These data indicate that enhanced sensitivity of central sympathetic pathways does not account for the enhanced SNS responses to LPS in ADX rats. Also, a CRF-related process appears to diminish renal sympathetic outflow in ADX rats.