Kyushu University Academic Staff Educational and Research Activities Database
List of Papers
Katayama Yuta Last modified date:2022.05.30

Assistant Professor / Department of Molecular and Cellular Biology / Medical Institute of Bioregulation

1. Makoto Habara, Yuki Sato, Takahiro Goshima, Hideyuki Shimizu, Yuta Katayama, Shunsuke Hanaki, Keisuke Maeda, Takahiro Masaki, Sayaka Nishikawa, Tatsuya Toyama, Midori Shimada, FKBP52 and FKBP51 differentially regulate the stability of estrogen receptor in breast cancer, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 10.1073/pnas.2110256119, 119, 15, 119, 15, 2022.04.
2. Chihiro Sakaguchi, Kazuya Ichihara, Akihiro Nita, Yuta Katayama, Keiichi I. Nakayama, Identification and characterization of novel proteins associated with CHD4, GENES TO CELLS, 10.1111/gtc.12909, 27, 1, 61-71, 27: 61-71, 2022.01.
3. Atsuki Kawamura, Yuta Katayama, Wataru Kakegawa, Daisuke Ino, Masaaki Nishiyama, Michisuke Yuzaki, Keiichi I Nakayama, The autism-associated protein CHD8 is required for cerebellar development and motor function, CELL REPORTS, 10.1016/j.celrep.2021.108932, 35, 1, 2021.04.
4. Akihiro Nita, Yoshiharu Muto, Yuta Katayama, Akinobu Matsumoto, Masaaki Nishiyama, Keiichi I Nakayama, The autism-related protein CHD8 contributes to the stemness and differentiation of mouse hematopoietic stem cells, CELL REPORTS, 10.1016/j.celrep.2021.108688, 34, 5, 2021.02.
5. Atsuki Kawamura, Yoshifumi Abe, Fumiko Seki, Yuta Katayama, Masaaki Nishiyama, Norio Takata, Kenji F Tanaka, Hideyuki Okano, Keiichi I Nakayama, Chd8 mutation in oligodendrocytes alters microstructure and functional connectivity in the mouse brain, MOLECULAR BRAIN, 10.1186/s13041-020-00699-x, 13, 1, 2020.11.
6. Kawamura Atsuki、Katayama Yuta、Nishiyama Masaaki、Shoji Hirotaka、Tokuoka Kota、Ueta Yoshifumi、Miyata Mariko、Isa Tadashi、Miyakawa Tsuyoshi、Hayashi-Takagi Akiko、Nakayama Keiichi I., Oligodendrocyte dysfunction due to Chd8 mutation gives rise to behavioral deficits in mice, Human Molecular Genetics, 10.1093/hmg/ddaa036, 29, 8, 1274-1291, 29: 1274-1291, 2020.06.
7. Yoshiharu Muto, Toshiro Moroishi, Kazuya Ichihara, Masaaki Nishiyama, Hideyuki Shimizu, Hidetoshi Eguchi, Kyoji Moriya, Kazuhiko Koike, Koshi Mimori, Masaki Mori, Yuta Katayama, Keiichi Nakayama, Disruption of FBXL5-mediated cellular iron homeostasis promotes liver carcinogenesis, Journal of Experimental Medicine, 10.1084/jem.20180900, 216, 4, 950-965, 2019.04, Hepatic iron overload is a risk factor for progression of hepatocellular carcinoma (HCC), although the molecular mechanisms underlying this association have remained unclear. We now show that the iron-sensing ubiquitin ligase FBXL5 is a previously unrecognized oncosuppressor in liver carcinogenesis in mice. Hepatocellular iron overload elicited by FBXL5 ablation gave rise to oxidative stress, tissue damage, inflammation, and compensatory proliferation of hepatocytes and to consequent promotion of liver carcinogenesis induced by exposure to a chemical carcinogen. The tumor-promoting outcome of FBXL5 deficiency in the liver was also found to be effective in a model of virus-induced HCC. FBXL5-deficient mice thus constitute the first genetically engineered mouse model of liver carcinogenesis promoted by iron overload. In addition, dysregulation of FBXL5-mediated cellular iron homeostasis was found to be associated with poor prognosis in human HCC, suggesting that FBXL5 plays a key role in defense against hepatocarcinogenesis..
8. Kelvin Hui, Yuta Katayama, Keiichi Nakayama, Jun Nomura, Takeshi Sakurai, Characterizing vulnerable brain areas and circuits in mouse models of autism
Towards understanding pathogenesis and new therapeutic approaches, Neuroscience and Biobehavioral Reviews, 10.1016/j.neubiorev.2018.08.001, 2018.01, Recent human genetics studies have identified many genetic variants that may be responsible for autism spectrum disorder (ASD). ASD mouse models with genetic modifications mimicking these rare genetic variants have provided invaluable mechanistic insights into the disruption of various biological processes and brain areas/circuitry affected in ASD patients. In this review, we begin by reviewing several mouse models for ASD-associated copy number variations (CNVs) to illustrate how they have been employed to establish causal links between their behavioral phenotypes and the affected genes. We then focus on studies using one of the principal behavioral abnormalities associated with ASD, social behavior, to identify the molecular and circuit-level deficits involved. Finally, we end by discussing other mouse models designed to probe how the disruption of specific biological processes such as autophagy and neurogenesis may contribute to ASD pathogenesis. By achieving a greater understanding of the pathophysiology and pathogenic mechanisms involved in ASD and related disorders, novel therapeutic strategies may be devised for ASD patients in the near future..
9. Hideo Hagihara, Vibeke S. Catts, Yuta Katayama, Hirotaka Shoji, Tsuyoshi Takagi, Freesia L. Huang, Akito Nakao, Yasuo Mori, Kuo Ping Huang, Shunsuke Ishii, Isabella A. Graef, Keiichi Nakayama, Cynthia Shannon Weickert, Tsuyoshi Miyakawa, Decreased Brain pH as a Shared Endophenotype of Psychiatric Disorders, Neuropsychopharmacology, 10.1038/npp.2017.167, 43, 3, 459-468, 2018.02, Although the brains of patients with schizophrenia and bipolar disorder exhibit decreased brain pH relative to those of healthy controls upon postmortem examination, it remains controversial whether this finding reflects a primary feature of the diseases or is a result of confounding factors such as medication and agonal state. To date, systematic investigation of brain pH has not been undertaken using animal models that can be studied without confounds inherent in human studies. In the present study, we first reevaluated the pH of the postmortem brains of patients with schizophrenia and bipolar disorder by conducting a meta-analysis of existing data sets from 10 studies. We then measured pH, lactate levels, and related metabolite levels in brain homogenates from five neurodevelopmental mouse models of psychiatric disorders, including schizophrenia, bipolar disorder, and autism spectrum disorder. All mice were drug naive with the same agonal state, postmortem interval, and age within each strain. Our meta-analysis revealed that brain pH was significantly lower in patients with schizophrenia and bipolar disorder than in control participants, even when a few potential confounding factors (postmortem interval, age, and history of antipsychotic use) were considered. In animal experiments, we observed significantly lower pH and higher lactate levels in the brains of model mice relative to controls, as well as a significant negative correlation between pH and lactate levels. Our findings suggest that lower pH associated with increased lactate levels is not a mere artifact, but rather implicated in the underlying pathophysiology of schizophrenia and bipolar disorder..
10. Yasuyuki Kita, Yuta Katayama, Taichi Shiraishi, Takeru Oka, Tetsuya Sato, Mikita Suyama, Yasuyuki Ohkawa, Keishi Miyata, Yuichi Oike, Michiko Shirane, Masaaki Nishiyama, Keiichi Nakayama, The Autism-Related Protein CHD8 Cooperates with C/EBPβ to Regulate Adipogenesis, Cell Reports, 10.1016/j.celrep.2018.04.050, 23, 7, 1988-2000, 2018.05, The gene encoding the chromatin remodeler CHD8 is the most frequently mutated gene in individuals with autism spectrum disorder (ASD). Heterozygous mutations in CHD8 give rise to ASD that is often accompanied by macrocephaly, gastrointestinal complaints, and slender habitus. Whereas most phenotypes of CHD8 haploinsufficiency likely result from delayed neurodevelopment, the mechanism underlying slender habitus has remained unknown. Here, we show that CHD8 interacts with CCAAT/enhancer-binding protein β (C/EBPβ) and promotes its transactivation activity during adipocyte differentiation. Adipogenesis was impaired in Chd8-deleted preadipocytes, with the upregulation of C/EBPα and peroxisome-proliferator-activated receptor γ (PPARγ), two master regulators of this process, being attenuated in mutant cells. Furthermore, mice with CHD8 ablation in white preadipocytes had a markedly reduced white adipose tissue mass. Our findings reveal a mode of C/EBPβ regulation by CHD8 during adipogenesis, with CHD8 deficiency resulting in a defect in the development of white adipose tissue. Kita et al. show that autism-related protein CHD8 is essential for adipogenesis and the development of white adipose tissue. Moreover, they demonstrate that CHD8 cooperates with C/EBPβ to regulate transactivation of the genes for C/EBPα and PPARγ during adipogenesis..
11. Yuta Katayama, Masaaki Nishiyama, Hirotaka Shoji, Yasuyuki Ohkawa, Atsuki Kawamura, Tetsuya Sato, Mikita Suyama, Toru Takumi, Tsuyoshi Miyakawa, Keiichi Nakayama, CHD8 haploinsufficiency results in autistic-like phenotypes in mice, Nature, 10.1038/nature19357, 537, 7622, 675-679, 2016.01, Autism spectrum disorder (ASD) comprises a range of neurodevelopmental disorders characterized by deficits in social interaction and communication as well as by restricted and repetitive behaviours. ASD has a strong genetic component with high heritability. Exome sequencing analysis has recently identified many de novo mutations in a variety of genes in individuals with ASD, with CHD8, a gene encoding a chromatin remodeller, being most frequently affected. Whether CHD8 mutations are causative for ASD and how they might establish ASD traits have remained unknown. Here we show that mice heterozygous for Chd8 mutations manifest ASD-like behavioural characteristics including increased anxiety, repetitive behaviour, and altered social behaviour. CHD8 haploinsufficiency did not result in prominent changes in the expression of a few specific genes but instead gave rise to small but global changes in gene expression in the mouse brain, reminiscent of those in the brains of patients with ASD. Gene set enrichment analysis revealed that neurodevelopment was delayed in the mutant mouse embryos. Furthermore, reduced expression of CHD8 was associated with abnormal activation of RE-1 silencing transcription factor (REST), which suppresses the transcription of many neuronal genes. REST activation was also observed in the brains of humans with ASD, and CHD8 was found to interact physically with REST in the mouse brain. Our results are thus consistent with the notion that CHD8 haploinsufficiency is a highly penetrant risk factor for ASD, with disease pathogenesis probably resulting from a delay in neurodevelopment..
12. Fumihiko Okumura, Yui Matsunaga, Yuta Katayama, Keiichi Nakayama, Shigetsugu Hatakeyama, TRIM8 modulates STAT3 activity through negative regulation of PIAS3, Journal of Cell Science, 10.1242/jcs.068981, 123, 13, 2238-2245, 2010.07, TRIM8 is a member of the protein family defined by the presence of a common domain structure composed of a tripartite motif: a RING-finger, one or two B-box domains and a coiled-coil motif. Here, we show that TRIM8 interacts with protein inhibitor of activated STAT3 (PIAS3), which inhibits IL-6-dependent activation of STAT3. Ectopic expression of TRIM8 cancels the negative effect of PIAS3 on STAT3, either by degradation of PIAS3 through the ubiquitin-proteasome pathway or exclusion of PIAS3 from the nucleus. Furthermore, expression of TRIM8 in NIH3T3 cells enhances Src-dependent tumorigenesis. These findings indicate that TRIM8 enhances the STAT3-dependent signal pathway by inhibiting the function of PIAS3..