ASB2 is a novel E3 ligase of SMAD9 required for cardiogenesis.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
29 11 2021
Historique:
received: 15 06 2021
accepted: 15 11 2021
entrez: 30 11 2021
pubmed: 1 12 2021
medline: 15 2 2022
Statut: epublish

Résumé

Cardiogenesis requires the orchestrated spatiotemporal tuning of BMP signalling upon the balance between induction and counter-acting suppression of the differentiation of the cardiac tissue. SMADs are key intracellular transducers and the selective degradation of SMADs by the ubiquitin-proteasome system is pivotal in the spatiotemporal tuning of BMP signalling. However, among three SMADs for BMP signalling, SMAD1/5/9, only the specific E3 ligase of SMAD9 remains poorly investigated. Here, we report for the first time that SMAD9, but not the other SMADs, is ubiquitylated by the E3 ligase ASB2 and targeted for proteasomal degradation. ASB2, as well as Smad9, is conserved among vertebrates. ASB2 expression was specific to the cardiac region from the very early stage of cardiac differentiation in embryogenesis of mouse. Knockdown of Asb2 in zebrafish resulted in a thinned ventricular wall and dilated ventricle, which were rescued by simultaneous knockdown of Smad9. Abundant Smad9 protein leads to dysregulated cardiac differentiation through a mechanism involving Tbx2, and the BMP signal conducted by Smad9 was downregulated under quantitative suppression of Smad9 by Asb2. Our findings demonstrate that ASB2 is the E3 ligase of SMAD9 and plays a pivotal role in cardiogenesis through regulating BMP signalling.

Identifiants

pubmed: 34845242
doi: 10.1038/s41598-021-02390-0
pii: 10.1038/s41598-021-02390-0
pmc: PMC8630118
doi:

Substances chimiques

Asb2 protein, mouse 0
ASB2 ubiqutin ligase, zebrafish 0
Bone Morphogenetic Proteins 0
Proteasome Endopeptidase Complex EC 3.4.25.1
Smad8 Protein 0
Smad9 protein, mouse 0
Suppressor of Cytokine Signaling Proteins 0
Ubiquitin 0
Ubiquitin-Protein Ligases EC 2.3.2.27
SMAD9 protein, zebrafish 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

23056

Informations de copyright

© 2021. The Author(s).

Références

Abdelwahid, E., Rice, D., Pelliniemi, L. J. & Jokinen, E. Overlapping and differential localization of Bmp-2, Bmp-4, Msx-2 and apoptosis in the endocardial cushion and adjacent tissues of the developing mouse heart. Cell Tissue Res. 305, 67–78 (2001).
pubmed: 11512673 doi: 10.1007/s004410100399
Gambaro, K., Aberdam, E., Virolle, T., Aberdam, D. & Rouleau, M. BMP-4 induces a Smad-dependent apoptotic cell death of mouse embryonic stem cell-derived neural precursors. Cell Death Differ. 13, 1075–1087 (2006).
pubmed: 16311513 doi: 10.1038/sj.cdd.4401799
Zou, H. & Niswander, L. Requirement for BMP signaling in interdigital apoptosis and scale formation. Science 272, 738–741 (1996).
pubmed: 8614838 doi: 10.1126/science.272.5262.738
Lamb, T. M. et al. Neural induction by the secreted polypeptide noggin. Science 262, 713–718 (1993).
pubmed: 8235591 doi: 10.1126/science.8235591
Sasai, Y. et al. Xenopus chordin: a novel dorsalizing factor activated by organizer-specific homeobox genes. Cell 79, 779–790 (1994).
pubmed: 8001117 pmcid: 3082463 doi: 10.1016/0092-8674(94)90068-X
Piccolo, S., Sasai, Y., Lu, B. & De Robertis, E. M. Dorsoventral patterning in Xenopus: inhibition of ventral signals by direct binding of chordin to BMP-4. Cell 86, 589–598 (1996).
pubmed: 8752213 pmcid: 3070603 doi: 10.1016/S0092-8674(00)80132-4
Zimmerman, L. B., De Jesus-Escobar, J. M. & Harland, R. M. The Spemann organizer signal noggin binds and inactivates bone morphogenetic protein 4. Cell 86, 599–606 (1996).
pubmed: 8752214 doi: 10.1016/S0092-8674(00)80133-6
Witty, A. D. et al. Generation of the epicardial lineage from human pluripotent stem cells. Nat. Biotechnol. 32, 1026–1035 (2014).
pubmed: 25240927 pmcid: 4192149 doi: 10.1038/nbt.3002
Iyer, D. et al. Robust derivation of epicardium and its differentiated smooth muscle cell progeny from human pluripotent stem cells. Development 142, 1528–1541 (2015).
pubmed: 25813541 pmcid: 4392600
Sun, B. et al. Bone morphogenetic protein-4 mediates cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. Hypertension 61, 352–360 (2013).
pubmed: 23248151 doi: 10.1161/HYPERTENSIONAHA.111.00562
Lim, D. A. et al. Noggin antagonizes BMP signaling to create a niche for adult neurogenesis. Neuron 28, 713–726 (2000).
pubmed: 11163261 doi: 10.1016/S0896-6273(00)00148-3
Hyzy, S. L., Olivares-Navarrete, R., Schwartz, Z. & Boyan, B. D. BMP2 induces osteoblast apoptosis in a maturation state and noggin-dependent manner. J. Cell. Biochem. 113, 3236–3245 (2012).
pubmed: 22628200 doi: 10.1002/jcb.24201
Onichtchouk, D. et al. Silencing of TGF-beta signalling by the pseudoreceptor BAMBI. Nature 401, 480–485 (1999).
pubmed: 10519551 doi: 10.1038/46794
Babitt, J. L. et al. Repulsive guidance molecule (RGMa), a DRAGON homologue, is a bone morphogenetic protein co-receptor. J. Biol. Chem. 280, 29820–29827 (2005).
pubmed: 15975920 doi: 10.1074/jbc.M503511200
Samad, T. A. et al. DRAGON, a bone morphogenetic protein co-receptor. J. Biol. Chem. 280, 14122–14129 (2005).
pubmed: 15671031 doi: 10.1074/jbc.M410034200
Xia, Y. et al. Repulsive guidance molecule RGMa alters utilization of bone morphogenetic protein (BMP) type II receptors by BMP2 and BMP4. J. Biol. Chem. 282, 18129–18140 (2007).
pubmed: 17472960 doi: 10.1074/jbc.M701679200
Itoh, S. & ten Dijke, P. Negative regulation of TGF-beta receptor/Smad signal transduction. Curr. Opin. Cell Biol. 19, 176–184 (2007).
pubmed: 17317136 doi: 10.1016/j.ceb.2007.02.015
Zhu, H., Kavsak, P., Abdollah, S., Wrana, J. L. & Thomsen, G. H. A SMAD ubiquitin ligase targets the BMP pathway and affects embryonic pattern formation. Nature 400, 687–693 (1999).
pubmed: 10458166 doi: 10.1038/23293
Lin, X., Liang, M. & Feng, X. H. Smurf2 is a ubiquitin E3 ligase mediating proteasome-dependent degradation of Smad2 in transforming growth factor-beta signaling. J. Biol. Chem. 275, 36818–36822 (2000).
pubmed: 11016919 doi: 10.1074/jbc.C000580200
Zhang, Y., Chang, C., Gehling, D. J., Hemmati-Brivanlou, A. & Derynck, R. Regulation of Smad degradation and activity by Smurf2, an E3 ubiquitin ligase. Proc. Natl. Acad. Sci. USA 98, 974–979 (2001).
pubmed: 11158580 pmcid: 14694 doi: 10.1073/pnas.98.3.974
Ebisawa, T. et al. Smurf1 interacts with transforming growth factor-beta type I receptor through Smad7 and induces receptor degradation. J. Biol. Chem. 276, 12477–12480 (2001).
pubmed: 11278251 doi: 10.1074/jbc.C100008200
Komuro, A. et al. Negative regulation of transforming growth factor-beta (TGF-beta) signaling by WW domain-containing protein 1 (WWP1). Oncogene 23, 6914–6923 (2004).
pubmed: 15221015 doi: 10.1038/sj.onc.1207885
Shi, W. et al. Overexpression of Smurf1 negatively regulates mouse embryonic lung branching morphogenesis by specifically reducing Smad1 and Smad5 proteins. Am. J. Physiol. Lung Cell Mol. Physiol. 286, L293-300 (2004).
pubmed: 14711801 doi: 10.1152/ajplung.00228.2003
Wei, C. Y., Wang, H. P., Zhu, Z. Y. & Sun, Y. H. Transcriptional factors smad1 and smad9 act redundantly to mediate zebrafish ventral specification downstream of smad5. J. Biol. Chem. 289, 6604–6618 (2014).
pubmed: 24488494 doi: 10.1074/jbc.M114.549758
Rual, J. F. et al. Towards a proteome-scale map of the human protein-protein interaction network. Nature 437, 1173–1178 (2005).
pubmed: 16189514 doi: 10.1038/nature04209
Arnold, S. J., Maretto, S., Islam, A., Bikoff, E. K. & Robertson, E. J. Dose-dependent Smad1, Smad5 and Smad8 signaling in the early mouse embryo. Dev. Biol. 296, 104–118 (2006).
pubmed: 16765933 pmcid: 7116376 doi: 10.1016/j.ydbio.2006.04.442
Monzen, K. et al. Bone morphogenetic proteins induce cardiomyocyte differentiation through the mitogen-activated protein kinase kinase kinase TAK1 and cardiac transcription factors Csx/Nkx-2.5 and GATA-4. Mol. Cell Biol. 19, 7096–7105 (1999).
pubmed: 10490646 pmcid: 84704 doi: 10.1128/MCB.19.10.7096
Blitz, I. L. & Cho, K. W. Finding partners: How BMPs select their targets. Dev. Dyn. 238, 1321–1331 (2009).
pubmed: 19441058 doi: 10.1002/dvdy.21984
Christoffels, V. M. et al. T-box transcription factor Tbx2 represses differentiation and formation of the cardiac chambers. Dev. Dyn. 229, 763–770 (2004).
pubmed: 15042700 doi: 10.1002/dvdy.10487
Harrelson, Z. et al. Tbx2 is essential for patterning the atrioventricular canal and for morphogenesis of the outflow tract during heart development. Development 131, 5041–5052 (2004).
pubmed: 15459098 doi: 10.1242/dev.01378
Shirai, M., Imanaka-Yoshida, K., Schneider, M. D., Schwartz, R. J. & Morisaki, T. T-box 2, a mediator of Bmp-Smad signaling, induced hyaluronan synthase 2 and Tgfbeta2 expression and endocardial cushion formation. Proc. Natl. Acad. Sci. USA 106, 18604–18609 (2009).
pubmed: 19846762 pmcid: 2773962 doi: 10.1073/pnas.0900635106
Yuasa, S. et al. Transient inhibition of BMP signaling by Noggin induces cardiomyocyte differentiation of mouse embryonic stem cells. Nat. Biotechnol. 23, 607–611 (2005).
pubmed: 15867910 doi: 10.1038/nbt1093
Chang, C. & Harland, R. M. Neural induction requires continued suppression of both Smad1 and Smad2 signals during gastrulation. Development 134, 3861–3872 (2007).
pubmed: 17933792 doi: 10.1242/dev.007179
Ladd, A. N., Yatskievych, T. A. & Antin, P. B. Regulation of avian cardiac myogenesis by activin/TGFbeta and bone morphogenetic proteins. Dev. Biol. 204, 407–419 (1998).
pubmed: 9882479 doi: 10.1006/dbio.1998.9094
Ying, S. X., Hussain, Z. J. & Zhang, Y. E. Smurf1 facilitates myogenic differentiation and antagonizes the bone morphogenetic protein-2-induced osteoblast conversion by targeting Smad5 for degradation. J. Biol. Chem. 278, 39029–39036 (2003).
pubmed: 12871975 doi: 10.1074/jbc.M301193200
Zhao, M. et al. Smurf1 inhibits osteoblast differentiation and bone formation in vitro and in vivo. J. Biol. Chem. 279, 12854–12859 (2004).
pubmed: 14701828 doi: 10.1074/jbc.M313294200
Massague, J., Seoane, J. & Wotton, D. Smad transcription factors. Genes Dev. 19, 2783–2810 (2005).
pubmed: 16322555 doi: 10.1101/gad.1350705
Sapkota, G., Alarcon, C., Spagnoli, F. M., Brivanlou, A. H. & Massague, J. Balancing BMP signaling through integrated inputs into the Smad1 linker. Mol. Cell 25, 441–454 (2007).
pubmed: 17289590 doi: 10.1016/j.molcel.2007.01.006
Wrighton, K. H., Lin, X. & Feng, X. H. Phospho-control of TGF-beta superfamily signaling. Cell Res. 19, 8–20 (2009).
pubmed: 19114991 doi: 10.1038/cr.2008.327
Schiffer, M., von Gersdorff, G., Bitzer, M., Susztak, K. & Bottinger, E. P. Smad proteins and transforming growth factor-beta signaling. Kidney Int. Suppl. 77, S45-52 (2000).
pubmed: 10997690 doi: 10.1046/j.1523-1755.2000.07708.x
Guo, X. et al. Axin and GSK3-control Smad3 protein stability and modulate TGF-signaling. Genes Dev. 22, 106–120 (2008).
pubmed: 18172167 pmcid: 2151009 doi: 10.1101/gad.1590908
Fuentealba, L. C. et al. Integrating patterning signals: Wnt/GSK3 regulates the duration of the BMP/Smad1 signal. Cell 131, 980–993 (2007).
pubmed: 18045539 pmcid: 2200633 doi: 10.1016/j.cell.2007.09.027
Kohroki, J. et al. ATRA-regulated Asb-2 gene induced in differentiation of HL-60 leukemia cells. FEBS Lett. 505, 223–228 (2001).
pubmed: 11566180 doi: 10.1016/S0014-5793(01)02829-0
Heuze, M. L. et al. ASB2 targets filamins A and B to proteasomal degradation. Blood 112, 5130–5140 (2008).
pubmed: 18799729 pmcid: 2597609 doi: 10.1182/blood-2007-12-128744
Bello, N. F. et al. The E3 ubiquitin ligase specificity subunit ASB2beta is a novel regulator of muscle differentiation that targets filamin B to proteasomal degradation. Cell Death Differ. 16, 921–932 (2009).
pubmed: 19300455 doi: 10.1038/cdd.2009.27
Metais, A. et al. Asb2alpha-Filamin A axis is essential for actin cytoskeleton remodeling during heart development. Circ. Res. 122, e34–e48 (2018).
pubmed: 29374072 doi: 10.1161/CIRCRESAHA.117.312015
Yamak, A. et al. Loss of Asb2 Impairs Cardiomyocyte Differentiation and Leads to Congenital Double Outlet Right Ventricle. iScience 23, 100959 (2020).
pubmed: 32179481 pmcid: 7078385 doi: 10.1016/j.isci.2020.100959
Huang, Z., Wang, D., Ihida-Stansbury, K., Jones, P. L. & Martin, J. F. Defective pulmonary vascular remodeling in Smad8 mutant mice. Hum. Mol. Genet. 18, 2791–2801 (2009).
pubmed: 19419974 pmcid: 2706683 doi: 10.1093/hmg/ddp214
Yamada, M., Revelli, J. P., Eichele, G., Barron, M. & Schwartz, R. J. Expression of chick Tbx-2, Tbx-3, and Tbx-5 genes during early heart development: evidence for BMP2 induction of Tbx2. Dev. Biol. 228, 95–105 (2000).
pubmed: 11087629 doi: 10.1006/dbio.2000.9927
Habets, P. E. et al. Cooperative action of Tbx2 and Nkx2.5 inhibits ANF expression in the atrioventricular canal: implications for cardiac chamber formation. Genes Dev 16, 1234–1246 (2002).
pubmed: 12023302 pmcid: 186286 doi: 10.1101/gad.222902
Stennard, F. A. & Harvey, R. P. T-box transcription factors and their roles in regulatory hierarchies in the developing heart. Development 132, 4897–4910 (2005).
pubmed: 16258075 doi: 10.1242/dev.02099

Auteurs

Kyung-Duk Min (KD)

Department of Clinical Research and Development, National Cerebral and Cardiovascular Center, 6-1 Kishibe- Shimmachi, Suita, Osaka, 564-8565, Japan.

Masanori Asakura (M)

Department of Clinical Research and Development, National Cerebral and Cardiovascular Center, 6-1 Kishibe- Shimmachi, Suita, Osaka, 564-8565, Japan.
Department of Cardiovascular and Renal Medicine, Hyogo College of Medicine, Hyogo, Japan.

Manabu Shirai (M)

Department of Bioscience, National Cerebral and Cardiovascular Center, Osaka, Japan.
Omics Research Center, National Cerebral and Cardiovascular Center, Osaka, Japan.

Satoru Yamazaki (S)

Department of Cell Biology, National Cerebral and Cardiovascular Center, Osaka, Japan.
Department of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Osaka, Japan.

Shin Ito (S)

Department of Clinical Research and Development, National Cerebral and Cardiovascular Center, 6-1 Kishibe- Shimmachi, Suita, Osaka, 564-8565, Japan.

Hai Ying Fu (HY)

Department of Clinical Research and Development, National Cerebral and Cardiovascular Center, 6-1 Kishibe- Shimmachi, Suita, Osaka, 564-8565, Japan.
Department of Cardiorenal and Cerebrovascular Medicine, Faculty of Medicine, Kagawa University, Kagawa, Japan.

Hiroshi Asanuma (H)

Department of Internal Medicine, Meiji University of Integrative Medicine, Kyoto, Japan.

Yoshihiro Asano (Y)

Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.

Tetsuo Minamino (T)

Department of Cardiorenal and Cerebrovascular Medicine, Faculty of Medicine, Kagawa University, Kagawa, Japan.

Seiji Takashima (S)

Department of Medical Biochemistry, Osaka University Graduate School of Medicine, Osaka, Japan.

Masafumi Kitakaze (M)

Department of Clinical Research and Development, National Cerebral and Cardiovascular Center, 6-1 Kishibe- Shimmachi, Suita, Osaka, 564-8565, Japan. kitakaze@zf6.so-net.ne.jp.
Hanwa Daini Senboku Hospital, Sakai, Osaka, Japan. kitakaze@zf6.so-net.ne.jp.

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