No abstract

Heritabilities and genetic correlations among growth‐related traits of two cultured strains (Rainbow Springs and Spring Valley) of rainbow trout Oncorhynchus mykiss were estimated using restricted maximum likelihood methods with a three‐generation pedigree. Heritability was high (>0·50 ± 0·03) for body mass and condition factor but moderate (0·35 ± 0·04) for age at sexual maturity in males. Body mass and age at sexual maturation were phenotypically correlated in the families of one experimental strain, Rainbow Springs, and had a positive genetic correlation (0·26 ± 0·03) across families from both test strains (Rainbow Springs and Spring Valley). This indicates that faster growing individuals were more likely to mature at 2 years of age than slower growing individuals in the two hatchery strains investigated. Microsatellite markers of body mass quantitative tract loci (QTL) were reconfirmed as being located on linkage groups B, G, N, 5 and new markers on Oi were detected. Some QTL effects were restricted to specific sampling dates suggesting temporal expression of QTL. QTL for condition factor were limited to linkage group G in both strains. Three suggestive QTL for precocious maturation mapped to similar regions as those for body mass in the Rainbow Springs families while no associations were evident in the Spring Valley families. The results suggest that these regions may play a role in the basis for genetic and phenotypic correlations between body mass and precocious maturation in this species.

Endogenous bioelectric signaling via changes in cellular resting potential (V mem ) is a key regulator of patterning during regeneration and embryogenesis in numerous model systems. Depolarization of V mem has been functionally implicated in dedifferentiation, tumorigenesis, anatomical re-specification, and appendage regeneration. However, no unbiased analyses have been performed to understand genome-wide transcriptional responses to V mem change in vivo. Moreover, it is unknown which genes or gene networks represent conserved targets of bioelectrical signaling across different patterning contexts and species. Here, we use microarray analysis to comparatively analyze transcriptional responses to V mem depolarization. We compare the response of the transcriptome during embryogenesis (Xenopus development), regeneration (axolotl regeneration), and stem cell differentiation (human mesenchymal stem cells in culture) to identify common networks across model species that are associated with depolarization. Both subnetwork enrichment and PANTHER analyses identified a number of key genetic modules as targets of V mem change, and also revealed important (well-conserved) commonalities in bioelectric signal transduction, despite highly diverse experimental contexts and species. Depolarization regulates specific transcriptional networks across all three germ layers (ectoderm, mesoderm, and endoderm) such as cell differentiation and apoptosis, and this information will be used for developing mechanistic models of bioelectric regulation of patterning. Moreover, our analysis reveals that V mem change regulates transcripts related to important disease pathways such as cancer and neurodegeneration, which may represent novel targets for emerging electroceutical therapies.

Since packaging of DNA in the chromatin structure restricts the accessibility for regulatory factors, chromatin remodeling is required to facilitate nuclear processes such as gene transcription, replication, and genome recombination. Many conserved non-enzymatic protein domains have been identified that contribute to the activities of multiprotein remodeling complexes. Here we identified a novel conserved protein domain in Eukaryota whose putative function may be in regulating chromatin remodeling. Since this domain is associated with a known SANT domain in several vertebrate proteins, we named it the SANTA (SANT Associated) domain. Sequence analysis showed that the SANTA domain is approximately a 90 amino acid module and likely composed of four central beta-sheets and three flanking alpha-helices. Many hydrophobic residues exhibited high conservation along the domain, implying a possible function in protein-protein interactions. The SANTA domain was identified in mammals, chicken, frog, fish, sea squirt, sea urchin, worms and plants. Furthermore, a phylogenetic tree of SANTA domains showed that one plant-specific duplication event happened in the Viridiplantae lineage.

Changes in tissue masses associated with egg production were investigated in female Zebra Finches Taeniopygia gutatta using dietary and hormonal manipulations. We tested three hypotheses: that changes in organ masses, (a) reflect utilisation of endogenous nutrient stores due to inadequate daily dietary intake, (b) involve changes in organ structure or ‘functional capacity’, and (c) are initiated by onset of reproductive development (e.g. elevated plasma estrogen or yolk precursor levels, oviduct growth). Pectoral muscle lean dry mass was 18–22% lower in breeding females at the 1‐egg stage compared to non‐breeders, and this was independent of nutritional plane, i.e. similar changes occurred in birds provided with supplemental protein or egg food. Heart lean dry mass was also lower (16%) in breeding females, but only in birds on a low‐quality seed diet, not in birds on supplemented diets. Decreases in total liver mass (14%) were due to changes in lipid content not lean dry mass, and were diet‐dependent. These results demonstrate that changes in organ masses associated with egg production are complex, and do not simply reflect a general mobilisation of stored protein. We discuss why there is no hypertrophy of biosynthetic or metabolic ‘machinery’ associated with egg production in birds (cf. reproducing mammals). Exogenous 17β‐estradiol induced plasma levels of yolk precursors typical of breeding birds, and initiated oviduct growth (to 31% of mature size). However, estradiol treatment caused no change in mass of pectoral muscle, heart or liver, demonstrating that there is no simple relationship between onset of reproductive development and associated tissue mass changes.

Two key inputs that regulate regeneration are the function of the immune system, and spatial gradients of transmembrane potential (V mem). Endogenous bioelectric signaling in somatic tissues during regenerative patterning is beginning to be understood, but its role in the context of immune response has never been investigated. Here, we show that V mem levels modulate innate immunity activity in Xenopus laevis embryos. We developed an assay in which X. laevis embryos are infected with a uropathogenic microorganism, in the presence or absence of reagents that modify V mem, prior to the ontogenesis of the adaptive immune system. General depolarization of the organism’s V mem by pharmacological or molecular genetic (ion channel misexpression) methods increased resistance to infection, while hyperpolarization made the embryos more susceptible to death by infection. Hyperpolarized specimens harbored a higher load of infectious microorganisms when compared to controls. We identified two mechanisms by which V mem mediates immune function: serotonergic signaling involving melanocytes and an increase in the number of primitive myeloid cells. Bioinformatics analysis of genes whose transcription is altered by depolarization revealed a number of immune system targets consistent with mammalian data. Remarkably, amputation of the tail bud potentiates systemic resistance to infection by increasing the number of peripheral myeloid cells, revealing an interplay of regenerative response, innate immunity, and bioelectric regulation. Our study identifies bioelectricity as a new mechanism by which innate immune response can be regulated in the context of infection or regeneration. V mem modulation using drugs already approved for human use could be exploited to improve resistance to infections in clinical settings.

No abstract

GABA is one of the most abundant neurotransmitters in the vertebrate central nervous system and is involved in neuroendocrine processes such as development, reproduction, feeding and stress. To examine the effect of GABA on gene expression in the brain, we used a cDNA macroarray containing 26 genes involved in GABA synaptic transmission (GABA receptor subunits, GABA transporters), reproduction (gonadotrophin-releasing hormone isoforms and oestrogen receptor alpha), feeding (neuropeptide Y and cholecystokinin), and stress [corticotrophin-releasing factor (CRF)]. To elevate GABA levels in the brain, we injected female goldfish with gamma-vinyl GABA (300 microg/g of body weight) (24 h), an irreversible inhibitor of the enzyme GABA transaminase (GABA-T). We found that increased levels of GABA in the hypothalamus resulted in a 2.2-fold down-regulation of GABA(A) receptor beta4 subunit mRNA. In the telencephalon, we found that increased GABA levels resulted in a 1.5-fold increase of CRF mRNA and a 1.8-fold decrease of GABA(A) receptor beta2 subunit mRNA. Increasing GABA in the hypothalamus and telencephalon of the goldfish did not significantly affect the mRNA abundance of genes involved in GABA synthesis (glutamic acid decarboxylase isoforms) and degradation (GABA-T), feeding, or reproduction. Our preliminary study suggests that the regulation of GABA receptor subunit mRNA expression by GABA may be a conserved evolutionary mechanism in vertebrates to modulate GABAergic synaptic transmission.