Genomic trajectories of a near-extinction event in the Chatham Island black robin
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ABSTRACT:
PROVIDER: PRJEB46470 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6335760.fastq.gz | Fastqsanger.gz | |||
| ERR6335770.fastq.gz | Fastqsanger.gz | |||
| ERR6335780.fastq.gz | Fastqsanger.gz | |||
| ERR6335790.fastq.gz | Fastqsanger.gz | |||
| ERR6335800.fastq.gz | Fastqsanger.gz |
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Project description:BackgroundUnderstanding the micro--evolutionary response of populations to demographic declines is a major goal in evolutionary and conservation biology. In small populations, genetic drift can lead to an accumulation of deleterious mutations, which will increase the risk of extinction. However, demographic recovery can still occur after extreme declines, suggesting that natural selection may purge deleterious mutations, even in extremely small populations. The Chatham Island black robin (Petroica traversi) is arguably the most inbred bird species in the world. It avoided imminent extinction in the early 1980s and after a remarkable recovery from a single pair, a second population was established and the two extant populations have evolved in complete isolation since then. Here, we analysed 52 modern and historical genomes to examine the genomic consequences of this extreme bottleneck and the subsequent translocation.ResultsWe found evidence for two-fold decline in heterozygosity and three- to four-fold increase in inbreeding in modern genomes. Moreover, there was partial support for temporal reduction in total load for detrimental variation. In contrast, compared to historical genomes, modern genomes showed a significantly higher realised load, reflecting the temporal increase in inbreeding. Furthermore, the translocation induced only small changes in the frequency of deleterious alleles, with the majority of detrimental variation being shared between the two populations.ConclusionOur results highlight the dynamics of mutational load in a species that recovered from the brink of extinction, and show rather limited temporal changes in mutational load. We hypothesise that ancestral purging may have been facilitated by population fragmentation and isolation on several islands for thousands of generations and may have already reduced much of the highly deleterious load well before human arrival and introduction of pests to the archipelago. The majority of fixed deleterious variation was shared between the modern populations, but translocation of individuals with low mutational load could possibly mitigate further fixation of high-frequency deleterious variation.
| S-EPMC9647977 | biostudies-literature
Project description:Extinction learning refers to the phenomenon that a previously learned response to an environmental stimulus, for example the expression of an aversive behavior upon exposure to a specific context, is reduced when the stimulus is repeatedly presented in the absence of a previously paired aversive event. Extinction of fear memories has been implicated with the treatment of anxiety disease but the molecular processes that underlie fear extinctionare only beginning to emerge. Here we show that fear extinction initiates up-regulation of hippocampal insulin-growth factor 2 (Igf2) and down-regulation of insulin-growth factor binding protein 7 (Igfbp7). In line with this observation we demonstrate that IGF2 facilitates fear extinction, while IGFBP7 impairs fear extinction in an IGF2-dependent manner. Furthermore, we identify one cellular substrate of altered IGF2-signaling during fear extinction. To this end we show that fear extinction-induced IGF2/IGFBP7-signaling promotes the survival of 17-19 day-old newborn hippocampal neurons. In conclusion, our data suggests that therapeutic strategies that enhance IGF2-signaling and adult neurogenesis might be suitable to treat disease linked to excessive fear memory. We employed mice to investigate fear extinction in the hippocampus-dependent contextual fear conditioning paradigm. To this end, male C57BL/6J mice were exposed to the fear conditioning box (context) followed by an electric foot-shock which elicits the acquisition of conditioned contextual fear. For extinction training animals were repeatedly reexposed to the conditioned context on consecutive days (24h interval) without receiving the footshockagain (extinction trial, E). This procedure eventually results in the decline of the aversive freezing behavior. Mice that were exposed to the conditioning context without receiving fear conditioning training served as control groups. To gain a better understanding of the molecular processes underlying fear extinction we performed a genome-wide analysis of the hippocampal transcriptome during fear extinction. In the employed paradigm fear extinction is a gradual process. To capture the longitudinal course of fear extinction we decided to perform hippocampal microarray analysis at two time points: (1) After the first extinction trial (E1) when animals display high levels of aversive freezing behavior and (2) at the extinction trial on which the freezing behavior was significantly reduced when compared to E1. This extinction trial, in the case of this experiment E5, we termed “extinction trial low freezing” (ELF). Mice that were exposed to the conditioning context without receiving fear conditioning training served as control groups (3). For all three groups we hybridized 5 samples (biological replicates).
2011-08-07 | E-GEOD-31063 | biostudies-arrayexpress
Project description:Extinction learning refers to the phenomenon that a previously learned response to an environmental stimulus, for example the expression of an aversive behavior upon exposure to a specific context, is reduced when the stimulus is repeatedly presented in the absence of a previously paired aversive event. Extinction of fear memories has been implicated with the treatment of anxiety disease but the molecular processes that underlie fear extinctionare only beginning to emerge. Here we show that fear extinction initiates up-regulation of hippocampal insulin-growth factor 2 (Igf2) and down-regulation of insulin-growth factor binding protein 7 (Igfbp7). In line with this observation we demonstrate that IGF2 facilitates fear extinction, while IGFBP7 impairs fear extinction in an IGF2-dependent manner. Furthermore, we identify one cellular substrate of altered IGF2-signaling during fear extinction. To this end we show that fear extinction-induced IGF2/IGFBP7-signaling promotes the survival of 17-19 day-old newborn hippocampal neurons. In conclusion, our data suggests that therapeutic strategies that enhance IGF2-signaling and adult neurogenesis might be suitable to treat disease linked to excessive fear memory.
2011-08-08 | GSE31063 | GEO
Project description:Dilution-to-extinction study Metagenome
| PRJNA864105 | ENA
Project description:A small animal population becomes extinct owing to demographic and environmental stochasticity after declining below the minimum viable population (MVP). However, the actual process of extinction derived by stochastic factors after crossing MVP has not been recorded for long-lived marine mammals. Here, we reconstructed the declining history of a small, isolated population of dugongs in Okinawa over 125 years. The initial population size of approximately 280-420 in the nineteenth century declined to approximately < 100 in 1917 because of overfishing, < 70 in 1979, 11 in 1997, 3 after 2006, and all known individuals disappeared or died by 2019. After 1979, a decline in the natural growth rate has led to extinction. Long-lived animals may persist for a few decades after the population falls below the MVP, at which time active conservation measures, such as captive breeding, should be implemented.
| S-EPMC9005736 | biostudies-literature
Project description:Trauma-related disorders arise from inefficient fear extinction and have immeasurable social and economic costs. Here, we characterized mouse phenotypes that spontaneously show individual differences in adaptive or maladaptive fear extinction and, before the traumatic experience, we found that specific morphological, electrophysiological and transcriptomic patterns of fear matrix pyramidal neurons predispose to trauma-related disorders. Finally, by using an optogenetic approach we showed the possibility to rescue the inefficient fear extinction activating fear matrix infralimbic pyramidal neurons
2023-06-02 | GSE209572 | GEO
Project description:There is a growing appreciation of the role of non-coding RNAs in the regulation of gene and protein expression. Long non-coding RNAs can modulate splicing by hybridizing with precursor messenger RNAs (pre-mRNAs) and influence RNA editing, mRNA stability, translation activation and microRNA-mRNA interactions by binding to mature mRNAs. LncRNAs are highly abundant in the brain and have been implicated in neurodevelopmental disorders. Long intergenic non-coding RNAs are the largest subclass of lncRNAs and play a crucial role in gene regulation. We used RNA sequencing and bioinformatic analyses to identify lincRNAs and their predicted mRNA targets associated with fear extinction that was induced by intra-hippocampally administered D-cycloserine in an animal model investigating the core phenotypes of PTSD. We identified 43 differentially expressed fear extinction related lincRNAs and 190 differentially expressed fear extinction related mRNAs. Eight of these lincRNAs were predicted to interact with and regulate 108 of these mRNAs and seven lincRNAs were predicted to interact with 22 of their pre-mRNA transcripts. On the basis of the functions of their target RNAs, we inferred that these lincRNAs bind to nucleotides, ribonucleotides and proteins and subsequently influence nervous system development, and morphology, immune system functioning, and are associated with nervous system and mental health disorders. Quantitative trait loci that overlapped with fear extinction related lincRNAs, included serum corticosterone level, neuroinflammation, anxiety, stress and despair related responses. This is the first study to identify lincRNAs and their RNA targets with a putative role in transcriptional regulation during fear extinction.
2020-03-01 | E-MTAB-8647 | biostudies-arrayexpress
Project description:To identify the differentially expressed gene in ikras tumors treated with Trametinib or Kras extinction.
2021-06-07 | GSE176241 | GEO
Project description:Neurobiological alterations seen in addiction amplify during abstinence and compromise relapse prevention. Cocaine use disorder (CUD) exemplifies this phenomenon in which reward regions such as nucleus accumbens (NAc) undergo withdrawal-associated modifications. While genome-wide transcriptional changes in NAc are linked to specific addiction phases, these have not been examined in a context- and NAc-subregion-specific manner during withdrawal vs. extinction. We used cocaine self-administration in rats combined with RNA-sequencing of NAc core and shell to transcriptionally profile withdrawal in the home-cage, in the previous drug context, or after extinction. As expected, home-cage withdrawal maintained drug seeking, whereas extinction reduced it. Conversely, withdrawal involving the drug context increased seeking. Bioinformatic analyses revealed specific gene expression patterns and networks associated with these states. Comparing NAc datasets of CUD patients highlighted conserved transcriptomic signatures with rats experiencing withdrawal in the drug context. Together, this work reveals fundamental mechanisms that can be targeted to attenuate relapse.
2025-01-13 | GSE264129 | GEO
Project description:We sought to understand the pathways involved in NRAS extinction over time using a doxycycline-dependent, inducible mouse model of melanoma. This data provides insights into the temporal dynamics of downstream NRAS signaling and helps to correlate differentially affected pathways. We used microarrays to determine which transcripts were affected by NRAS-Q61K extinction at 24, 48, and 72 hours after doxycycline withdrawal. This data was used in support of a separate dataset submitted to GEO entitled Comparison of the genetic extinction of NRAS to pharmacological MEK inhibition in an inducible mouse model of melanoma. The iNRAS-475 mouse melanoma cell line was injected intradermally into nude mice which were fed 2mg/ml doxycycline water. Tumors were allowed to reach 200-500mm3 after 6 weeks. Doxycyline was then withdrawn from the diet and tumors harvested at 24, 48, and 72 hours post-withdrawal.
2012-08-08 | E-GEOD-39985 | biostudies-arrayexpress