Project description:Brains from female Astatotilapia burtoni were sampled at four timepoints throughout the reproductive cycle with the primary goal of comparing transcriptome profiles at the different stages and identifying genes and networks involved in parental and fasting behaviors.
Project description:Metriaclima estherae, Protomelas similis, Rhamphochromis "chilingali", and Astatotilapia tweddlei genomic DNA hybridized with Astatotilapia burtoni genomic DNA 2 Metriaclima estherae vs Astatotilapia burtoni, 2 Protomelas similis vs Astatotilapia burtoni, 2 Rhamphochromis "chilingali" vs Astatotilapia burtoni, and 2 Astatotilapia tweddlei vs Astatotilapia burtoni hybs, all in balanced dye swaps
Project description:Metriaclima estherae, Protomelas similis, Rhamphochromis "chilingali", and Astatotilapia tweddlei genomic DNA hybridized with Astatotilapia burtoni genomic DNA
Project description:Astatotilapia burtoni males change their startle behavior in accordance with changes in a socially-mediated phenotypic state. When dominant (DOM), males are brightly colored, isolated from the school and startle readily in response to an auditory pulse. When subordinate (SUB), males are cryptically colored, school and startle less frequently. We hypothesize that the difference in startle responsiveness is governed by serotonergic modulation on the command-like Mauthner cells (M-cells). We used the selective serotonin receptor subtype 2 (5HTR2) antagonist ketanserin to show that serotonin receptors can modulate startle frequency and that the behavioral difference correlates with differences in electrophysiological recordings of M-cells. Specifically, SUB males have a higher serotonergic tone and demonstrate, by behavior and electrophysiological properties, increased sensitivity to 5-HT manipulations compared to DOMs. Immunohistochemistry for serotonin is present around the M-cells. Furthermore, we identified serotonin receptor transcripts in A. burtoni and used single-cell transcriptomics to determine the presence or absence of specific receptor subtypes in the M-cells. Microarray analysis of M-cell samples shows that the neuron’s transcriptome is relatively stable in individuals of different social status. These results are consistent with a role for serotonin in modulating the behavioral response to sensory stimuli in an ecologically-relevant manner through inhibitory interneurons, which establish the membrane resistance of the M-cell before the auditory stimulus. Simple loop with dye-swap containing 6 arrays from 2 sources with 3 biological replicates per source (3 M-cell and 3 whole brain samples).
Project description:Comparison of social dominance phenotypes induced in the cichlid A. burtoni females with the goal of comparing to other gene expression profiles of social dominance Used platform GPL928 In many species, under varying ecological conditions, social interactions among individuals result in the formation dominance hierarchies. Despite general similarities, there are substantial differences across species, populations, environments, life stages, sexes, and individuals. Understanding the proximate mechanisms of this variation is an important step toward understanding the evolution of social behavior. However, physiological changes associated with dominance such as gonadal maturation and somatic growth, often complicate efforts to identify the specific underlying mechanisms. We demonstrate complementary analysis tools to allow a comparative approach to high-throughput expression profiling that allow us to both test a priori hypotheses and generate new hypotheses about the mechanisms and evolution of social dominance. Using experimental manipulation to produce female dominance hierarchies in the cichlid A. burtoni, heralded as a genomic model of social dominance, we generate gene lists, and assess molecular gene modules. We demonstrate a general pattern of “masculinization” of the female neural gene expression profile and compare expression biases between male and female dominance hierarchies. Using a threshold-free approach to identify correlation throughout gene ranked lists, we query previously published datasets from maternal behavior, alternative reproductive tactics, cooperative breeding and sex-role reversal to describe correlations among neural gene expression profiles. These complementary approaches capitalize on the high-throughput gene expression profiling from similar behavioral phenotypes in order to address the mechanism associated with social dominance behavioral phenotypes.
Project description:Astatotilapia burtoni males change their startle behavior in accordance with changes in a socially-mediated phenotypic state. When dominant (DOM), males are brightly colored, isolated from the school and startle readily in response to an auditory pulse. When subordinate (SUB), males are cryptically colored, school and startle less frequently. We hypothesize that the difference in startle responsiveness is governed by serotonergic modulation on the command-like Mauthner cells (M-cells). We used the selective serotonin receptor subtype 2 (5HTR2) antagonist ketanserin to show that serotonin receptors can modulate startle frequency and that the behavioral difference correlates with differences in electrophysiological recordings of M-cells. Specifically, SUB males have a higher serotonergic tone and demonstrate, by behavior and electrophysiological properties, increased sensitivity to 5-HT manipulations compared to DOMs. Immunohistochemistry for serotonin is present around the M-cells. Furthermore, we identified serotonin receptor transcripts in A. burtoni and used single-cell transcriptomics to determine the presence or absence of specific receptor subtypes in the M-cells. Microarray analysis of M-cell samples shows that the neuron’s transcriptome is relatively stable in individuals of different social status. These results are consistent with a role for serotonin in modulating the behavioral response to sensory stimuli in an ecologically-relevant manner through inhibitory interneurons, which establish the membrane resistance of the M-cell before the auditory stimulus.