Sho Ohta's research while affiliated with The University of Tokyo and other places
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Publications (10)
The resistance to transcription factor-mediated reprogramming into pluripotent stem cells is one of the distinctive features of cancer cells. Here we dissect the profiles of reprogramming factor binding and the subsequent transcriptional response in cancer cells to reveal its underlying mechanisms. Using clear cell sarcomas (CCSs), we show that the...
β cells have a limited capacity for regeneration, which predisposes towards diabetes. Here, we show that, of the MYC family members, Mycl plays a key role in proliferation of pancreatic endocrine cells. Genetic ablation of Mycl causes a reduction in the proliferation of pancreatic endocrine cells in neonatal mice. By contrast, the expression of Myc...
The cyclin-dependent kinase inhibitor p16Ink4a plays a central role in cellular senescence in vitro. Although previous studies suggested cellular senescence is integrated in the systemic mechanisms of organismal aging, the localization and the dynamics of p16Ink4a in tissues remain poorly understood, which hinders uncovering the role of p16Ink4a un...
In vivo reprogramming provokes a wide range of cell fate conversion. Here, we discover that in vivo induction of higher levels of OSKM in mouse somatic cells leads to increased expression of primordial germ cell (PGC)-related genes and provokes genome-wide erasure of genomic imprinting, which takes place exclusively in PGCs. Moreover, the in vivo O...
PTBP1, a well-conserved RNA-binding protein, regulates cellular development by tuning posttranscriptional mRNA modification such as alternative splicing (AS) or mRNA stabilization. We previously revealed that the loss of Ptbp1 in spermatogonia causes the dysregulation of spermatogenesis, but the molecular mechanisms by which PTBP1 regulates spermat...
De novo establishment of DNA methylation is accomplished by DNMT3A and DNMT3B. Here, we analyze de novo DNA methylation in mouse embryonic fibroblasts (2i-MEFs) derived from DNA-hypomethylated 2i/L ES cells with genetic ablation of Dnmt3a or Dnmt3b. We identify 355 and 333 uniquely unmethylated genes in Dnmt3a and Dnmt3b knockout (KO) 2i-MEFs, resp...
Clear cell sarcoma (CCS) is a rare soft tissue sarcoma caused by the EWS/ATF1 fusion gene. Here, we established induced pluripotent stem cells (iPSCs) from EWS/ATF1-controllable murine CCS cells harboring sarcoma-associated genetic abnormalities. Sarcoma-iPSC mice develop secondary sarcomas immediately after EWS/ATF1 induction, but only in soft tis...
ES cell (ESC) identity is stably maintained through the coordinated regulation of transcription factors and chromatin structure. SMARCB1, also known as INI1, SNF5, BAF47, is one of the subunits of SWI/SNF (BAF) complexes that play a crucial role in regulating gene expression by controlling chromatin dynamics. Genetic ablation of Smarcb1 in mice lea...
CpG islands (CGIs)including those at imprinting control regions (ICRs)are protected from de novo methylation in somatic cells. However, many cancers often exhibit CGI hypermethylation, implying that the machinery is impaired in cancer cells. Here, we conducted a comprehensive analysis of CGI methylation during somatic cell reprogramming. Although m...
Atypical teratoid/rhabdoid tumor (AT/RT), which harbors SMARCB1 mutation and exhibits a characteristic histology of rhabdoid cells, has a poor prognosis because of the lack of effective treatments. Here, we establish human SMARCB1-deficient pluripotent stem cells (hPSCs). SMARCB1-deficient hPSC-derived neural progenitor-like cells (NPLCs) efficient...
Citations
... Many breakthrough results in reprogramming have been achieved both in vitro and in vivo, including restoring vision and improving the regenerative ability of various organs (Ocampo et al., 2016;Wang et al., 2021;Hishida et al., 2022). However, in certain normal and specific environments, this process can cause potential carcinogenic risks and unexpected loss of tissue function (possibly due to a lack of perfect control over the reprogramming process) (Ito et al., 2022). In this article, we review the emergence, development, and application of reprogramming in diseases. ...
... Alternatively, as MEN1 controls multiple epigenetic and signaling pathways [96], its inactivation in α-cells may also activate specific reprogramming mechanisms, perhaps linked to proliferation. In a more recent study, inducible and temporally controlled mosaic whole-body misexpression of the Mycl oncogene in mice caused islet hyperplasia without tumor development [97]. This sophisticated transgenic system also allowed inducible α-cell tracing using the Gcg-CreERT2 transgene. ...
... Eliminating SCs has proven to be a highly effective way of mitigating and even reversing disease in pre-clinical models of aging (Baker et al., 2011;Saccon et al., 2021;Wang L et al., 2022a;Chandra et al., 2022). Transgenic mouse models of SC identification and elimination are a powerful tool in measuring senescence burden within tissues (Baker et al., 2011;Xu et al., 2018;Yousefzadeh et al., 2019;Wang B et al., 2021;Shimada-Takayama et al., 2022). Senolytics have been used as pharmacological interventions for selective elimination of SCs in both genetically and nongenetically modified animals. ...
... In the present case, copy number variation analysis revealed DMRT1 loss and 12p gain. DMRT1, expressed in primordial germ cells, is known to drive the reprogramming and propagation of tumor cells, which have the capacity to induce pluripotent stem cells, leading to the development of cancer that resembles human germ cell tumors [13]. Dmrt1 acts as a dose-sensitive tumor suppressor gene in 129Sv mice, and loss of Dmrt1 has been shown to cause a high incidence of testicular teratomas in mice of the 129Sv strain [14]. ...
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... The cardiac anomalies observed in Foxp1 null mice embryos closely resemble those found in various types of congenital heart disease in humans [63]. In line with our report, Foxp1 gene has been identified as a target for de novo methylation by DNMT3A during mammalian development in mouse embryonic stem cells [64]. Moreover, functional gene analysis using the WebGestalt tool [65] revealed downregulated genes TPM2 (Log2 Fold change = − 1.3) and TGFBR3 (Log2 Fold change = − 0.73) which are associated with aortic aneurysms. ...
... C.H. Wei et al. be related to SMARCB1′s role in regulating differentiation through chromatin remodeling and transcriptional regulation. In mouse embryonic stem cells, SMARCB1 deficiency caused impaired differentiation during embryonic development in vivo with retention of pluripotent state (Sakakura et al., 2019). Lastly, another unique aspect of this case report is the repeated number of NGS tests our patient had received, which produced significant financial toxicity to the patient and to our healthcare system. ...
... In induced pluripotent stem cell models (iPSCs) derived from CSS, the inducible expression of the fusion oncogene EWS-ATF1 is sufficient for the formation of sarcomas in chimeric mice in a celltype-dependent manner (Komura et al., 2019). Indeed, despite the expression of EWS-ATF1 in a high variety of tissues, secondary sarcomas preferentially occur in soft tissues in these CSS initiation models. ...
... These modifications result in the functional silencing of various genes, providing potential molecular indicators for PsC and a deeper understanding of its root causes. PsC cells frequently employ promoter hypermethylation to suppress genes, facilitating the progression and maintenance of the cancerous characteristics 64 . This silencing affects a range of tumorsuppressor genes related to hormone signaling, DNA repair, cell adhesion, cell-cycle control, and programmed cell death 65 . ...
... An atypical teratoid/rhabdoid tumor (ATRT) originates as a malignant rhabdoid tumor of the central nervous system. Its cellular origin is largely unknown, perhaps early neural progenitor cells (NPCs) [1,2]. ATRT predominantly affects children and infants with biallelic inactivation of a tumor suppressor gene SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily B, member 1 (SMARCB1) [3][4][5]. ...
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