Lysine demethylase 7a regulates murine anterior-posterior development by modulating the transcription of Hox gene cluster

Research output: Contribution to journal › Journal article › Research › peer-review

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Lysine demethylase 7a regulates murine anterior-posterior development by modulating the transcription of Hox gene cluster. / Higashijima, Yoshiki; Nagai, Nao; Yamamoto, Masamichi; Kitazawa, Taro; Kawamura, Yumiko K.; Taguchi, Akashi; Nakada, Natsuko; Nangaku, Masaomi; Furukawa, Tetsushi; Aburatani, Hiroyuki; Kurihara, Hiroki; Wada, Youichiro; Kanki, Yasuharu.

In: Communications Biology , Vol. 3, No. 1, 725, 2020.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Higashijima, Y, Nagai, N, Yamamoto, M, Kitazawa, T, Kawamura, YK, Taguchi, A, Nakada, N, Nangaku, M, Furukawa, T, Aburatani, H, Kurihara, H, Wada, Y & Kanki, Y 2020, 'Lysine demethylase 7a regulates murine anterior-posterior development by modulating the transcription of Hox gene cluster', Communications Biology , vol. 3, no. 1, 725. https://doi.org/10.1038/s42003-020-01456-5

APA

Higashijima, Y., Nagai, N., Yamamoto, M., Kitazawa, T., Kawamura, Y. K., Taguchi, A., Nakada, N., Nangaku, M., Furukawa, T., Aburatani, H., Kurihara, H., Wada, Y., & Kanki, Y. (2020). Lysine demethylase 7a regulates murine anterior-posterior development by modulating the transcription of Hox gene cluster. Communications Biology , 3(1), [725]. https://doi.org/10.1038/s42003-020-01456-5

Vancouver

Higashijima Y, Nagai N, Yamamoto M, Kitazawa T, Kawamura YK, Taguchi A et al. Lysine demethylase 7a regulates murine anterior-posterior development by modulating the transcription of Hox gene cluster. Communications Biology . 2020;3(1). 725. https://doi.org/10.1038/s42003-020-01456-5

Author

Higashijima, Yoshiki ; Nagai, Nao ; Yamamoto, Masamichi ; Kitazawa, Taro ; Kawamura, Yumiko K. ; Taguchi, Akashi ; Nakada, Natsuko ; Nangaku, Masaomi ; Furukawa, Tetsushi ; Aburatani, Hiroyuki ; Kurihara, Hiroki ; Wada, Youichiro ; Kanki, Yasuharu. / Lysine demethylase 7a regulates murine anterior-posterior development by modulating the transcription of Hox gene cluster. In: Communications Biology . 2020 ; Vol. 3, No. 1.

Bibtex

@article{1efd163fd63d450c976064e98c47b24f,
title = "Lysine demethylase 7a regulates murine anterior-posterior development by modulating the transcription of Hox gene cluster",
abstract = "Higashijima et al show that mice lacking the Kdm7a demethylase exhibits anterior homeotic transformation of the axial skeleton and downregulation of posterior Hox gene transcription and these changes are associated with increased H3K9me2 at posterior Hox loci. These findings provide insights into the epigenetic control of Hox-mediated patterning in embryogenesis.Temporal and spatial colinear expression of the Hox genes determines the specification of positional identities during vertebrate development. Post-translational modifications of histones contribute to transcriptional regulation. Lysine demethylase 7A (Kdm7a) demethylates lysine 9 or 27 di-methylation of histone H3 (H3K9me2, H3K27me2) and participates in the transcriptional activation of developmental genes. However, the role of Kdm7a during mouse embryonic development remains to be elucidated. Herein, we show that Kdm7a(-/-) mouse exhibits an anterior homeotic transformation of the axial skeleton, including an increased number of presacral elements. Importantly, posterior Hox genes (caudally from Hox9) are specifically downregulated in the Kdm7a(-/-) embryo, which correlates with increased levels of H3K9me2, not H3K27me2. These observations suggest that Kdm7a controls the transcription of posterior Hox genes, likely via its demethylating activity, and thereby regulating the murine anterior-posterior development. Such epigenetic regulatory mechanisms may be harnessed for proper control of coordinate body patterning in vertebrates.",
keywords = "HISTONE METHYLTRANSFERASE, METHYLATION, EXPRESSION, SPECIFICATION, DYNAMICS, COMPLEX, G9A",
author = "Yoshiki Higashijima and Nao Nagai and Masamichi Yamamoto and Taro Kitazawa and Kawamura, {Yumiko K.} and Akashi Taguchi and Natsuko Nakada and Masaomi Nangaku and Tetsushi Furukawa and Hiroyuki Aburatani and Hiroki Kurihara and Youichiro Wada and Yasuharu Kanki",
year = "2020",
doi = "10.1038/s42003-020-01456-5",
language = "English",
volume = "3",
journal = "Communications Biology",
issn = "2399-3642",
publisher = "nature publishing group",
number = "1",

}

RIS

TY - JOUR

T1 - Lysine demethylase 7a regulates murine anterior-posterior development by modulating the transcription of Hox gene cluster

AU - Higashijima, Yoshiki

AU - Nagai, Nao

AU - Yamamoto, Masamichi

AU - Kitazawa, Taro

AU - Kawamura, Yumiko K.

AU - Taguchi, Akashi

AU - Nakada, Natsuko

AU - Nangaku, Masaomi

AU - Furukawa, Tetsushi

AU - Aburatani, Hiroyuki

AU - Kurihara, Hiroki

AU - Wada, Youichiro

AU - Kanki, Yasuharu

PY - 2020

Y1 - 2020

N2 - Higashijima et al show that mice lacking the Kdm7a demethylase exhibits anterior homeotic transformation of the axial skeleton and downregulation of posterior Hox gene transcription and these changes are associated with increased H3K9me2 at posterior Hox loci. These findings provide insights into the epigenetic control of Hox-mediated patterning in embryogenesis.Temporal and spatial colinear expression of the Hox genes determines the specification of positional identities during vertebrate development. Post-translational modifications of histones contribute to transcriptional regulation. Lysine demethylase 7A (Kdm7a) demethylates lysine 9 or 27 di-methylation of histone H3 (H3K9me2, H3K27me2) and participates in the transcriptional activation of developmental genes. However, the role of Kdm7a during mouse embryonic development remains to be elucidated. Herein, we show that Kdm7a(-/-) mouse exhibits an anterior homeotic transformation of the axial skeleton, including an increased number of presacral elements. Importantly, posterior Hox genes (caudally from Hox9) are specifically downregulated in the Kdm7a(-/-) embryo, which correlates with increased levels of H3K9me2, not H3K27me2. These observations suggest that Kdm7a controls the transcription of posterior Hox genes, likely via its demethylating activity, and thereby regulating the murine anterior-posterior development. Such epigenetic regulatory mechanisms may be harnessed for proper control of coordinate body patterning in vertebrates.

AB - Higashijima et al show that mice lacking the Kdm7a demethylase exhibits anterior homeotic transformation of the axial skeleton and downregulation of posterior Hox gene transcription and these changes are associated with increased H3K9me2 at posterior Hox loci. These findings provide insights into the epigenetic control of Hox-mediated patterning in embryogenesis.Temporal and spatial colinear expression of the Hox genes determines the specification of positional identities during vertebrate development. Post-translational modifications of histones contribute to transcriptional regulation. Lysine demethylase 7A (Kdm7a) demethylates lysine 9 or 27 di-methylation of histone H3 (H3K9me2, H3K27me2) and participates in the transcriptional activation of developmental genes. However, the role of Kdm7a during mouse embryonic development remains to be elucidated. Herein, we show that Kdm7a(-/-) mouse exhibits an anterior homeotic transformation of the axial skeleton, including an increased number of presacral elements. Importantly, posterior Hox genes (caudally from Hox9) are specifically downregulated in the Kdm7a(-/-) embryo, which correlates with increased levels of H3K9me2, not H3K27me2. These observations suggest that Kdm7a controls the transcription of posterior Hox genes, likely via its demethylating activity, and thereby regulating the murine anterior-posterior development. Such epigenetic regulatory mechanisms may be harnessed for proper control of coordinate body patterning in vertebrates.

KW - HISTONE METHYLTRANSFERASE

KW - METHYLATION

KW - EXPRESSION

KW - SPECIFICATION

KW - DYNAMICS

KW - COMPLEX

KW - G9A

U2 - 10.1038/s42003-020-01456-5

DO - 10.1038/s42003-020-01456-5

M3 - Journal article

C2 - 33257809

VL - 3

JO - Communications Biology

JF - Communications Biology

SN - 2399-3642

IS - 1

M1 - 725

ER -

ID: 253403985