Idotea baltica
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA871071 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21146600.fastq.gz | Fastqsanger.gz | |||
| SRR21146700.fastq.gz | Fastqsanger.gz | |||
| SRR21146601.fastq.gz | Fastqsanger.gz | |||
| SRR21146701.fastq.gz | Fastqsanger.gz | |||
| SRR21146602.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 214 |
Similar Datasets
Project description:Idotea baltica transcriptome and diet-specific gene expression
| PRJNA451082 | ENA
Project description:Hyposalinity as a selective agent in the littoral mesoherbivore Idotea balthica
| PRJNA668696 | ENA
Project description:Strong spatial genetic structure in a crustacean herbivore highlights the need for local considerations in Baltic Sea biodiversity management
| PRJNA551577 | ENA
Project description:How environmentally induced traits become genetically stabilized during evolution remains a central question in biology. The teleost Astyanax mexicanus, comprising surface (SF) and cave (CF) morphotypes, provides a powerful system to link environmentally induced traits with evolved phenotypes. Here, we integrate morphometric, physiological, and transcriptomic analyses to investigate how sustained darkness reshapes phenotypic plasticity across generations. We show that plastic responses in SF are rapidly modified after only two generations of dark rearing (2dSF). Morphological changes in 2dSF are highly heterogeneous: some traits shift toward cavefish values, while others overshoot them, and key traits such as eye size and pigmentation respond in the opposite direction, indicating widespread maladaptive plasticity. In contrast, CF exhibit limited environmental responsiveness, consistent with canalized phenotypes. Traits exhibiting maladaptive plasticity in SF tend to be canalized in CF, suggesting that maladaptive responses are preferentially reduced during evolution. At the molecular level, transcriptional plasticity declines sharply from SF to 2dSF and is nearly absent in CF, suggesting rapid loss of environmental responsiveness. Gene expression analyses further reveal a mixture of maladaptive and adaptive trajectories. Most transcriptional changes in 2dSF deviate from cavefish expression patterns, including those related to visual function, consistent with maladaptive morphological trends. However, a subset of genes involved in lipid metabolism and heme homeostasis shows stepwise shifts from SF through 2dSF to CF, consistent with adaptive accommodation. Notably, anesthesia resistance increases in 2dSF to levels comparable to CF within only two generations, demonstrating rapid accommodation in neural traits. Together, our results show that plastic phenotypes are initially heterogeneous but are rapidly reshaped across generations, with maladaptive components reduced and adaptive components stabilized. This process bridges immediate plasticity and long-term evolutionary change, providing empirical support for phenotypic accommodation as a mechanism facilitating rapid adaptation and highlighting how plasticity can biasing evolutionary trajectories during the colonization of extreme environments.
2026-05-08 | GSE324281 | GEO
Project description:Idotea baltica isolate:IB14FIS37 Genome sequencing and assembly
| PRJNA599581 | ENA
Project description:Animals learn and adapt to environmental changes. However, neural plasticity can also become maladaptive, leading to neurological and psychiatric disorders. How do we use known molecular mechanisms to harness the power of neural plasticity to prevent and treat diseases? Consolidating learning is known to require new protein synthesis. We found that mRNA m6A modifications and the RNA-binding protein YTHDF1 are required for molecular, cellular, and behavioral adaptations in response to environmental changes. Deletion of Ythdf1 in dopamine D1- or D2 receptor-expressing neurons selectively impaired D1- or D2-dependent learning, respectively, including both adaptive and maladaptive learning. This highlights YTHDF1 as a potential therapeutic target for preventing pathological plasticity. YTHDF1 recognizes m6A modifications on transcripts and regulates their translation. Elevated cAMP triggered increased protein synthesis in control striatal neurons but not in Ythdf1-deficient neurons. Behaviorally, cell-type-specific Ythdf1 deletion resembled learning phenotypes caused by deletion of the m6A methyltransferase gene Mettl14, suggesting YTHDF1 as the main mediator of m6A-dependent regulation in the striatum.
2026-04-01 | GSE326611 | GEO
Project description:Brain myeloid cells accumulate neutral lipids in multiple human neurodegenerative disorders and relevant mouse models. These neutral lipids are often assumed to be contained in lipid droplets (LDs), and ‘LD-high microglia’ have generally been characterized as maladaptive. While a number of studies have been performed in cell culture and Drosophila models to characterize glial LD dynamics, it is still unclear what roles microglial LD biogenesis play in mammalian tauopathy. To address this question, we induced the deletion of diacylglycerol acyltransferases 1 and 2 (DGATs), enzymes critical for LD formation via triglyceride (TAG) synthesis, from microglia in the PS19 mouse model of tauopathy. We observed that microglial DGAT double KO exacerbated neurodegeneration, induced behavioral deficits, and increased the abundance of brain cholesteryl esters in male PS19 mice. Myeloid cell lipid accumulations appeared to largely localize to endosomes/lysosomes not LDs in PS19 mice at baseline and this phenotype was exacerbated upon DGAT KO. Our results suggest that microglial DGAT-dependent TAG/LD biogenesis is adaptive in advanced tauopathy. Furthermore, the bulk of the lipid accumulation in brain myeloid cells may not correspond to true LDs in this tauopathy model, which has important implications for the development of lipid-modulating therapies for neurodegenerative diseases.
2025-11-17 | E-MTAB-16169 | biostudies-arrayexpress
Project description:The kidney tubules have tremendous capacity to repair after acute injury, however, pathways guiding adaptive and maladaptive (fibrotic) repair are poorly understood. We developed a model of adaptive and maladaptive kidney regeneration by titrating ischemic injury dose. We performed detailed biochemical and histological analysis and profiled transcriptomic changes at bulk and single-cell level in >110,000 cells over time. Our analysis highlighted kidney proximal tubule (PT) cells as key susceptible cells to injury. Adaptive PT repair correlated with fatty acid oxidation and oxidative phosphorylation. We identified a specific maladaptive/profibrotic PT cluster after long ischemia. These cells expressed proinflammatory and profibrotic cytokines and myeloid cell chemotactic factor. Druggability analysis highlighted pyroptosis and ferroptosis as vulnerable pathways in these profibrotic cells. Pharmacological targeting of pyroptosis/ferroptosis in animal model, pushed cells towards adaptive repair and successfully reduced fibrosis. In summary, our single-cell analysis defined key differences in adaptive and maladaptive repair and identified druggable pathways for pharmacological intervention to prevent kidney fibrosis.
2021-07-21 | GSE180420 | GEO
Project description:Transcriptional profiling of human adaptive and maladaptive right ventricular remodeling
| PRJNA1005692 | ENA