Resultados de investigación

Este anexo incluye información relevante no incluida en el libro impreso., This compilation encompasses all records of inland water animals and plants in Madrid County over the years. It is an appendix to the book "Ecología acuática de Madrid", published by Editorial CSIC in 2020., Peer reviewed

Contents: Repo Contents. -- System Requirements. -- Installation Guide. -- Demo. -- License. -- Issues. -- Citation, Peer reviewed

Expression profiling by high throughput sequencing. -- To delve deeper into the biological mechanisms implicated in the MIA effects on neurodevelopment processes, we have generated neural stem cell lines from fetuses carried by pregnant mice treated with Poly I:C with the aim of investigating the alterations that persist in cultured neurons derived from the differentiation of these neural progenitors., To undertake a comprehensive examination of the molecular mechanisms governing the alterations induced by maternal immune activation (MIA) during gestation that impacts the subsequent neurodevelopment of progeny, we have devised an in vitro model based on neural stem cells (NSCs) sourced from fetuses carried by animals subjected to Poly I:C treatment. These neural progenitors demonstrate proliferative properties and can be effectively differentiated into both neurons and glial cells. Through transcriptomic, proteomic, and phosphoproteomic analyses conducted on these cellular models, in conjunction with counterparts from control treatments, discernible shifts in the expression levels of a specific subset of proteins implicated in neuronal function were elucidated. Noteworthy is the absence of congruence between these alterations and the transcriptomic findings, suggesting a potential dysregulation at the level of protein translation. Furthermore, a discernible discrepancy in the basal phosphorylation of proteins was observed between differentiated cells from both experimental groups, particularly within proteins associated with cytoskeletal architecture and synaptic functionality, notably those belonging to the MAP family. These observed alterations were found to correlate with changes in neuronal function, particularly with respect to synaptic plasticity and the establishment of neuronal synapses, thereby reaffirming previous assertions regarding the potential impact of MAP2 function modulation via its phosphorylation state on neuronal structure and function., Peer reviewed

Expression profiling by high throughput sequencing, We dissected hippocampus from WT and Daam1-MIC_KO adult mice and perform RNA-seq, To investigate the impact of Daam1 microexon removal on hippocampal function, we have generated RNA-seq data from adult male mice. Actin cytoskeleton dynamics is crucial for neurogenesis and neuronal function. Precise quantitative and qualitative regulation of actin polymerization is achieved by multiple actin-binding proteins, among which formins are particularly versatile. Here, we investigate how neuronal-specific splicing expands formin's functional diversity in the brain. We uncovered a highly conserved microexon in DAAM1 that extends the linker region of its FH2 domain, leading to remarkable changes in actin polymerization rates and structure. Microexon deletion causes neuritogenesis defects and increased calcium influx in in vitro differentiated mouse neurons, and mice carrying this deletion exhibit deficient long-term memory formation. These memory defects were associated with higher activity of DAAM1's interactor RhoA, increased ARC protein levels, postsynaptic deficiencies, fewer dendritic spines and impaired long-term potentiation. In summary, precise post-transcriptional regulation of DAAM1's FH2 domain is a novel mechanism for modulating actin polymerization in neural spinesneurons and is essential for proper brain function., Peer reviewed

Sampled and measured for AMS using the KLY-3S Kappabridge (AGICO, Czech Republic) and processed with the Anisoft 5.1.01 software (Chadima et al., 2018)., This study was funded by Project UKRIA-4D (PID2019-104693GB-I00) of the Spanish Ministry of Science and Innovation,, Peer reviewed

Sampling, stepwise demagnetization and measurement of the natural remanent magnetization. - Methods for processing the data: Characteristic components directions (ChRM) were calculated by principal component analyses (PCA, Kirschvink, 1980) after they were identified through visual inspection of orthogonal demagnetization plots (Zijderveld, 1967) using the VPD software (Ramón et al., 2017)., Peer reviewed

Kdm1af/f, Kdm5cf/f and CamKIIα-CreERT2 mouse strains have been previously described , they are available at public repositories (Jackson Lab stock #23969; MMRRC stock 066789-UCD; and EMMA EM:02125, respectively). Mice were maintained on a C57BL/6J genetic background. The recombinant protein CreERT2 is dependent on tamoxifen (TMX) administration, and its expression is restricted to principal neurons of the forebrain, where CamKIIα is expressed. CaMKIIα–driven, TMX induced Cre recombination results in the elimination of exons 5 and 6 in Kdm1af/f and exons 11 and 12 in Kdm5cf/f . Mice were 2 to 3-month-old at the time of TMX administration., Loss or reduced expression of lysine demethylases (KDMs) is linked to neurodevelopmental disorders and intellectual disability. Given the phenotypic similarities between KDM1A and KDM5C deficient mice, and the convergence of both enzymes in maintaining a repressive state via H3K4 demethylation, we examined their functional interaction using double-inducible, forebrain-specific knockouts (dKDM-ifKOs). These mice showed transcriptional and epigenetic dysregulation beyond the additive effects of individual knockouts, including stronger ectopic expression of non-neuronal genes in hippocampal neurons. Thousands of de novo H3K4me3-enriched regions emerged, indicating synergistic disruption of chromatin regulation. In line with these molecular changes, dKDM-ifKOs displayed more severe behavioral impairments than the single ifKOs, along with altered hippocampal expression of ion channels and increased excitability of CA1 pyramidal neurons. These findings underscore the joint role of ID-linked KDMs in regulating cell-type-specific gene silencing and H3K4 methylation levels to safeguard neuronal identity and responsiveness, as well as cognitive function, Peer reviewed

Kdm1af/f, Kdm5cf/f and CamKIIα-CreERT2 mouse strains have been previously described , they are available at public repositories (Jackson Lab stock #23969; MMRRC stock 066789-UCD; and EMMA EM:02125, respectively). Mice were maintained on a C57BL/6J genetic background. The recombinant protein CreERT2 is dependent on tamoxifen (TMX) administration, and its expression is restricted to principal neurons of the forebrain, where CamKIIα is expressed. CaMKIIα–driven, TMX induced Cre recombination results in the elimination of exons 5 and 6 in Kdm1af/f and exons 11 and 12 in Kdm5cf/f . Mice were 2 to 3-month-old at the time of TMX administration., Loss or reduced expression of lysine demethylases (KDMs) is linked to neurodevelopmental disorders and intellectual disability. Given the phenotypic similarities between KDM1A and KDM5C deficient mice, and the convergence of both enzymes in maintaining a repressive state via H3K4 demethylation, we examined their functional interaction using double-inducible, forebrain-specific knockouts (dKDM-ifKOs). These mice showed transcriptional and epigenetic dysregulation beyond the additive effects of individual knockouts, including stronger ectopic expression of non-neuronal genes in hippocampal neurons. Thousands of de novo H3K4me3-enriched regions emerged, indicating synergistic disruption of chromatin regulation. In line with these molecular changes, dKDM-ifKOs displayed more severe behavioral impairments than the single ifKOs, along with altered hippocampal expression of ion channels and increased excitability of CA1 pyramidal neurons. These findings underscore the joint role of ID-linked KDMs in regulating cell-type-specific gene silencing and H3K4 methylation levels to safeguard neuronal identity and responsiveness, as well as cognitive function, Peer reviewed

Kdm5cf/f, and CamKIIα-CreERT2 mouse strains are available at public repositories (MMRRC stock 066789-UCD; and EMMA EM:02125, respectively). Mice were maintained on a C57BL/6J genetic background. The recombinant protein CreERT2 is dependent on tamoxifen (TMX) administration, and its expression is restricted to principal neurons of the forebrain, where CamKIIα is expressed. CaMKIIα–driven, TMX induced Cre recombination results in the elimination of exons 11 and 12 in Kdm5cf/f . Mice were 2 to 3-month-old at the time of TMX administration., Loss or reduced expression of lysine demethylases (KDMs) is linked to neurodevelopmental disorders and intellectual disability. Given the phenotypic similarities between KDM1A and KDM5C deficient mice, and the convergence of both enzymes in maintaining a repressive state via H3K4 demethylation, we examined their functional interaction using double-inducible, forebrain-specific knockouts (dKDM-ifKOs). These mice showed transcriptional and epigenetic dysregulation beyond the additive effects of individual knockouts, including stronger ectopic expression of non-neuronal genes in hippocampal neurons. Thousands of de novo H3K4me3-enriched regions emerged, indicating synergistic disruption of chromatin regulation. In line with these molecular changes, dKDM-ifKOs displayed more severe behavioral impairments than the single ifKOs, along with altered hippocampal expression of ion channels and increased excitability of CA1 pyramidal neurons. These findings underscore the joint role of ID-linked KDMs in regulating cell-type-specific gene silencing and H3K4 methylation levels to safeguard neuronal identity and responsiveness, as well as cognitive function, Peer reviewed

The study included a total of 39 blood samples, comprising 23 from de novo, drug-naïve Parkinson’s disease (PD) patients and 16 from healthy, age- and sex-matched controls. Following quality control assessments, one sample was excluded due to failing labeling control thresholds, resulting in a final dataset of 38 samples. Each patient represented a biological replicate. Peripheral Blood Mononuclear Cells (PBMCs) were isolated, and RNA was extracted and assessed for integrity before transcriptome analysis using the Clariom S Array (Affymetrix). Data preprocessing involved normalization and filtering, leading to a final dataset of 18,091 probes. -- Expression profiling by array, This study investigated gene expression differences in Parkinson’s disease (PD) using blood samples from 23 newly diagnosed, drug-naïve PD patients and 16 healthy controls recruited from two hospitals in Spain. Participants met diagnostic criteria for early-stage PD (Hoehn and Yahr I-II) and had no family history of the disease. Ethical approval and informed consent were obtained. Peripheral Blood Mononuclear Cells (PBMCs) were isolated, frozen, and processed for RNA extraction. RNA integrity was assessed before whole transcriptome analysis using the Clariom S Array (Affymetrix). Data processing was conducted in R using BioConductor packages. Quality control measures led to the exclusion of one sample, and data were normalized using Robust Multi-array Average (RMA). Lowly expressed genes and probes not mapping to known genes were filtered out, resulting in 38 samples with 18,091 probes, Peer reviewed