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Proteomic dataset of MECP2-deficient and wild-type human brain organoids under spaceflight and ground conditions

ABSTRACT: This dataset presents deep proteomic profiles of human brain organoids cultured aboard the International Space Station (ISS) and on Earth. We analyzed MECP2-deficient (Q83X) and isogenic wild-type control (WT83) organoids exposed to spaceflight and ground conditions for 30 days. Using LC-MS/MS on an Orbitrap Astral mass spectrometer, we confidently identified 56,639 peptides mapping to approximately 6,000 protein groups. The Q83X line models Rett syndrome, carrying a nonsense mutation that produces a severely truncated MeCP2 protein lacking critical functional domains. This unique dataset enables investigation of how spaceflight environment and MECP2 deficiency interact to affect human neural development, offering applications for understanding astronaut health risks and neurodevelopmental disorder mechanisms.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Paulo Carvalho

LAB HEAD: ALysson Muotri

PROVIDER: PXD069807 | Pride | 2026-02-09

REPOSITORIES: Pride

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			Action	DRS
	20250622_DDA_400ng_Tube26_Ground_QX_Plate2_RowE_Column8.raw	Raw
	20250622_DDA_400ng_Tube27_Ground_QX_Plate2_RowE_Column9.raw	Raw
	20250622_DDA_400ng_Tube28_Ground_QX_Plate2_RowE_Column10.raw	Raw
	20250622_DDA_400ng_Tube32_Ground_WT83_Plate2_RowF_Column8.raw	Raw
	20250622_DDA_400ng_Tube33_Ground_WT83_Plate2_RowF_Column9.raw	Raw

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MeCP2 regulates telencephalic development in human cerebral organoids

Project description:Human cerebral organoids and telencephalic assembloids derived from iPSC lines: isogenic control and harboring MeCP2 variants associated with Rett Syndrome.

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MeCP2 heterochromatin organization is modulated by arginine methylation and serine phosphorylation

Project description:Rett syndrome is a human intellectual disability disorder that is associated with mutations in the X-linked MECP2 gene. Theepigenetic reader MeCP2 binds to methylated cytosines on the DNA and regulates chromatin organization. We have shownpreviously that MECP2 Rett syndrome missense mutations are impaired in chromatin binding and heterochromatinreorganization. Here, we performed a proteomics analysis of post-translational modifications of MeCP2 isolated from adult mousebrain. We show that MeCP2 carries various post-translational modifications, among them phosphorylation on S80 and S421, whichlead to minor changes in either heterochromatin binding kinetics or clustering. We found that MeCP2 is (di)methylated on severalarginines and that this modification alters heterochromatin organization. Interestingly, we identified the Rett syndrome mutationsite R106 as a dimethylation site. In addition, co-expression of protein arginine methyltransferases 1 and 6 lead to a decrease ofheterochromatin clustering. Altogether, we identified and validated novel modifications of MeCP2 in the brain and show that thesecan modulate its ability to bind as well as reorganize heterochromatin, which may play a role in the pathology of Rett syndrome.

2022-10-15 | PXD033696 | Pride

Transcriptome analysis of a MECP2 conditional KO mouse model

Project description:Rett syndrome is a severe neurodevelopmental condition that rsults primarily from mutations in the MECP2 gene. MECP2 is known to function as both a transcriptional activator and transcriptional repressor. However, it remains unclear how transcriptional dysregulation resulting from MECP2 mutations lead to the Rett syndrome phenotype. Multiple mouse models have been generated to investigate the function of MECP2 in vivo. Remarkably, despite the neurodevelopmental phenotype characteristic of Rett syndrome, temporal conditional MECP2 knock-out mouse models with MECP2 deletion induced postnatally recapitulate the Rett-syndrome-like phenotype in mouse. Here we investigated gene expression changes in 22-weeks old mice following conditional MECP knock-out at 12 weeks by RNA-sequencing. Consistent with previous data, we identify mild gene expression changes following MECP2 knock-out. These data could prove valuable in future studies comparing conditional MECP2 knock-out at distinct time points and in additional brain regions, and can also serve for investigating alternative splicing changes resulting from MECP2 conditional deletion.

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Transcriptional dysregulation in a Mecp2 methyl-binding domain point mutant model (Mecp2 G118E)

Project description:We recently identified a mutation in the methyl-binding domain of MECP2 (MECP2 G118E) in a male patient with Rett syndrome. To ask whether this mutation conferred similar molecular dysregulation as observed in previous mouse models of Rett syndrome, we generated a knockin mouse model of this mutation and collected the cortex for RNA-sequencing.

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Cell type specific expression data from Mecp2 null mice

Project description:Human methyl-CpG-binding protein 2 (MeCP2) disruption causes Rett syndrome, an autistic disease prevalent in females. Previous microarray expression profiling studies using tissue homogenate samples from mouse model of the Rett syndrome revealed only modest changes in expression caused by the loss of Mecp2, making it difficult to identify etiology of the Rett syndrome. Here, we carried out cell type specific genome wide expression profiling of Mecp2 null mice in three neuronal cell types. We found a hot spot of Mecp2 affected genes in chromosome 11B3 syntenic to human chromosome 17p13 which has known associations to mental retardation. We also found Mecp2 affected genes are almost non-overlapping between cell types. Cell-adhesion category of genes, however, are commonly overrepresented, suggesting a possible etiology of Rett syndrome Keywords: cell type comparison, disease state analysis, genetic modification Transgenic mice lines which label subpopulations of neurons (G42: fast spiking Parvarbumin positive interneurons, YFPH: layer 5 thick tufted pyramidal neurons, TH: tyrosine hydroxylase positive locus coeruleus neurons) were used to obtain cell type specific expression profiles on Affymetrix microarrays. Females which carry Mecp2 null alleles (and one of the fluorescent alleles) were crossed with males (which may or may not carry one of the fluorescent alleles depending on whether the female has one or not). Male offsprings at around age P40 which carry fluorescent allele and Mecp2 null allele were used for experiments. Littermate males which carry fluorescent allele but not Mecp2 null allele were used for controls. 3 or 4 biological replicates were done for each condition.

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Genome-wide Analysis Reveals Mecp2-dependent Regulation of MicroRNAs in a Mouse Model of Rett Syndrome

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MeCP2 is a microsatellite binding protein that protects CA repeats from nucleosome invasion

Project description:The Rett syndrome protein MeCP2 was described as a methyl-CpG-binding protein, but its exact function remains unknown. Here we show that MeCP2 is a microsatellite binding protein that specifically recognizes hydroxymethylated CA repeats. Depletion of MeCP2 alters chromatin organization of CA repeats and lamina-associated domains and results in nucleosome accumulation on CA repeats and genome-wide transcriptional dysregulation. The structure of MeCP2 in complex with a hydroxymethylated CA repeat reveals a characteristic DNA shape, with significantly modified geometry at the 5-hydroxymethylcytosine, which is recognized specifically by Arg133, a key residue whose mutation causes Rett syndrome. Our work identifies MeCP2 as a microsatellite DNA binding protein that targets the 5hmC-modified CA-rich strand and maintains genome regions nucleosome-free, suggesting a role for MeCP2 dysfunction in Rett syndrome.

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MeCP2 is a microsatellite binding protein that protects CA repeats from nucleosome invasion

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