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Kdm3b haploinsufficiency impairs the consolidation of cerebellum-dependent optokinetic response memory in mice

ABSTRACT: Bulk RNA samples were recruited from GCE of the cerebellar vermis. We obtained two WT and two Kdm3b+/- mice samples for RNA-sequencing analysis. After trimming low-quality bases, the sequence reads were aligned using the STAR algorithm. Then, we quantified gene expression using the StringTie, resulting 16,447 genes expressed in cerebellum tissues.

ORGANISM(S): Mus musculus

PROVIDER: GSE173255 | GEO | 2021/04/26

REPOSITORIES: GEO

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Kdm3b haploinsufficiency impairs the consolidation of cerebellum-dependent motor memory in mice.

Project description:Histone modifications are a key mechanism underlying the epigenetic regulation of gene expression, which is critically involved in the consolidation of multiple forms of memory. However, the roles of histone modifications in cerebellum-dependent motor learning and memory are not well understood. To test whether changes in histone methylation are involved in cerebellar learning, we used heterozygous Kdm3b knockout (Kdm3b+/-) mice, which show reduced lysine 9 on histone 3 (H3K9) demethylase activity. H3K9 di-methylation is significantly increased selectively in the granule cell layer of the cerebellum of Kdm3b+/- mice. In the cerebellum-dependent optokinetic response (OKR) learning, Kdm3b+/- mice show deficits in memory consolidation, whereas they are normal in basal oculomotor performance and OKR acquisition. In addition, RNA-seq analyses revealed that the expression levels of several plasticity-related genes were altered in the mutant cerebellum. Our study suggests that active regulation of histone methylation is critical for the consolidation of cerebellar motor memory.

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Kdm3b haploinsufficiency impairs the consolidation of cerebellum-dependent optokinetic response memory in mice

Project description:Kdm3b haploinsufficiency impairs the consolidation of cerebellum-dependent optokinetic response memory in mice

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Reorganization of H3K9me heterochromatin leads the neuronal impairment via the cascading destruction of KDM3B-centered epigenomic network

Project description:Histone H3K9 methylated heterochromatin silences repetitive non-coding sequences and lineage-specific genes during development, but how tissue-specific genes escape from heterochromatin in differentiated cells is unclear. Here, we examine age-dependent transcriptomic profiling of terminally differentiated mouse retina to identify epigenetic regulators involved in heterochromatin reorganization. The single-cell RNA sequencing analysis reveal a gradual downregulation of Kdm3b in cone photoreceptors during aging. Disruption of Kdm3b (Kdm3b+/-) of 12-month-old mouse retina leads to the decreasing number of cones via apoptosis, and it changes the morphology of cone ribbon synapses. Integration of transcriptome with epigenomic analysis in Kdm3b+/- retinas demonstrate gains of heterochromatin feature in synapse assembly and vesicle transport genes that are downregulated via the accumulation of H3K9me1/2. Contrary, losses of heterochromatin in apoptotic genes exacerbated retinal neurodegeneration. We propose that KDM3B-centered epigenomic network is crucial for balancing of cone photoreceptor homeostasis via the modulation of gene-set specific heterochromatin features during aging.

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Pro‐inflammatory activation of microglia in the cerebellum hyperexcites Purkinje cells to trigger ataxia

Project description:Specific medications to combat cerebellar ataxias, a group of debilitating movement disorders characterized by difficulty with walking, balance and coordination. Notably, cerebellar microglial activation appears to be a common feature in different types of ataxic patients and rodent models. However, the causal link between the activation of microglia in the cerebellum and ataxias remains inconclusive. In the present study, using a classic mouse model of cerebellar ataxia induced by 3-acetylpyridine (3-AP), we find a early-onset and long-lasting microglial activation accompanied by neuronal loss and dysfunction in the cerebellum. Transcriptome and behavior analyses indicate that microglial depletion in 3-AP ataxic mice decreases neuroinflammatory response in the cerebellum and rescues the ataxic motor symptoms including motor incoordination, gait abnormality, and locomotor dysfunction. Moreover, specific chemogenetic activation of cerebellar microglia in the vermis by M3D(Gq), a designer receptor exclusively activated by designer drugs (DREADDs), directly induces an expression of pro-inflammatory cytokines and aggravates ataxic motor deficits of 3-AP mice. On the contrary, inhibition of cerebellar microglial activation by M4D(Gi) or minocycline reduces the production of pro-inflammatory cytokines including TNF-α and alleviates motor deficits. Furthermore, blockage of TNF-α signaling attenuates the microglial-triggered hyperactivity of Purkinje cells (PCs). These results suggest that cerebellar microglial activation aggravates neuroinflammatory response, and subsequently induces dysfunction of PCs, which in turn triggers ataxic motor deficits. Our findings thus reveal a causal relationship between pro-inflammatory activation of cerebellar microglia and the ataxic motor symptoms, which may offer novel evidence for therapeutic intervention for cerebellar ataxias by targeting microglia and microglia-derived inflammatory mediators.

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Systematic characterization of epigenetic modifying enzymes identifies KDM3B as a key regulator in castration resistant prostate cancer

Project description:Androgen deprivation therapy (ADT) is the standard care for prostate cancer patients who fail surgery and radiotherapy. While initially effective, the cancer almost always recurs into a more aggressive Castration Resistant Prostate Cancer (CRPC). Despite the existing evidence on the role of epigenetic modifiers in CRPC, only a handful of enzymes have been tested. In this study, we conducted a systematic shRNA library screen, focusing of epigenetic modifiers linked to stem-cell reprogramming, in LNCaP-abl cells, a model of CRPC. Amongst the shRNA hits, KDM3B, a histone H3K9 demethylase, was identified to have the most significant anti-proliferative effect on LNCaP-abl cells. KDM3B CRISPR/Cas9 knockout phenocopied the shRNA treatment, proving the observed phenotype was not due to shRNA off-target effects. Interestingly, this decrease in proliferation was remarkably specific to androgen-independent cells. Additionally, genetic rescue experiment showed that only enzymatically active KDM3B recovers the phenotype. No alterations in the cell cycle distribution or expression of AR downstream effectors were observed, but RNASeq revealed subtle changes in the genes expression profile for cells treated with KDM3A shRNA, including in metabolome-related enzymes such as ARG2, RDH11. However, metabolomic analysis in KDM3B knockout cells showed little change overall compared to untreated cells. Interestingly, we observed a decrease in the availability of amino acids in the absence of KDM3B which requires further investigation. Overall, our studies are the first ones to show the specificity of KDM3B in CRPC.

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