Aging-induced pseudouridine synthase 10 impairs hematopoietic stem cells
Aged hematopoietic stem cells (HSC) exhibit compromised reconstitution capacity and differentiation-bias towards myeloid lineage, however, the molecular mechanism behind it remains not fully understood. In this study, we observed that the expression of pseudouridine (Ψ) synthase 10 is increased in a...
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| Published in | Haematologica (Roma) Vol. 108; no. 10; pp. 2677 - 2689 |
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| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Italy
Fondazione Ferrata Storti
01.10.2023
Ferrata Storti Foundation |
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| Abstract | Aged hematopoietic stem cells (HSC) exhibit compromised reconstitution capacity and differentiation-bias towards myeloid lineage, however, the molecular mechanism behind it remains not fully understood. In this study, we observed that the expression of pseudouridine (Ψ) synthase 10 is increased in aged hematopoietic stem and progenitor cells (HSPC) and enforced protein of Ψ synthase 10 (PUS10) recapitulates the phenotype of aged HSC, which is not achieved by its Ψ synthase activity. Consistently, we observed no difference of transcribed RNA pseudouridylation profile between young and aged HSPC. No significant alteration of hematopoietic homeostasis and HSC function is observed in young Pus10-/- mice, while aged Pus10-/- mice exhibit mild alteration of hematopoietic homeostasis and HSC function. Moreover, we observed that PUS10 is ubiquitinated by E3 ubiquitin ligase CRL4DCAF1 complex and the increase of PUS10 in aged HSPC is due to aging-declined CRL4DCAF1- mediated ubiquitination degradation signaling. Taken together, this study for the first time evaluated the role of PUS10 in HSC aging and function, and provided a novel insight into HSC rejuvenation and its clinical application. |
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| AbstractList | Aged hematopoietic stem cells (HSCs) exhibit compromised reconstitution capacity and differentiation-bias towards myeloid lineage. While, the molecular mechanism behind it remains not fully understood. In this study, we observed that the expression of pseudouridine (Ψ) synthase 10 is increased in aged hematopoietic stem and progenitor cells (HSPCs) and enforced PUS10 recapitulates the phenotype of aged HSCs, which is not achieved by its Ψ synthase activity. Consistently, we observed no difference of tRNA pseudouridylation profile between young and aged HSPCs. No significant alteration of hematopoietic homeostasis and HSC function is observed in young Pus10-/- mice, while aged Pus10-/-mice exhibit mild alteration of hematopoietic homeostasis and HSC function. Moreover, we observed that PUS10 is ubiquitinated by E3 ubiquitin ligase CRL4DCAF1 complex and the increase of PUS10 in aged HSPCs is due to aging-declined CRL4DCAF1-mediated ubiquitination degradation signaling. Taken together, this study for the first time evaluated the role of PUS10 in HSC aging and function, and provided novel insight for HSC rejuvenation and clinical application. Aged hematopoietic stem cells (HSC) exhibit compromised reconstitution capacity and differentiation-bias towards myeloid lineage, however, the molecular mechanism behind it remains not fully understood. In this study, we observed that the expression of pseudouridine (Ψ) synthase 10 is increased in aged hematopoietic stem and progenitor cells (HSPC) and enforced protein of Ψ synthase 10 (PUS10) recapitulates the phenotype of aged HSC, which is not achieved by its Ψ synthase activity. Consistently, we observed no difference of transcribed RNA pseudouridylation profile between young and aged HSPC. No significant alteration of hematopoietic homeostasis and HSC function is observed in young Pus10-/- mice, while aged Pus10-/- mice exhibit mild alteration of hematopoietic homeostasis and HSC function. Moreover, we observed that PUS10 is ubiquitinated by E3 ubiquitin ligase CRL4DCAF1 complex and the increase of PUS10 in aged HSPC is due to aging-declined CRL4DCAF1- mediated ubiquitination degradation signaling. Taken together, this study for the first time evaluated the role of PUS10 in HSC aging and function, and provided a novel insight into HSC rejuvenation and its clinical application. Aged hematopoietic stem cells (HSC) exhibit compromised reconstitution capacity and differentiation-bias towards myeloid lineage, however, the molecular mechanism behind it remains not fully understood. In this study, we observed that the expression of pseudouridine (Ψ) synthase 10 is increased in aged hematopoietic stem and progenitor cells (HSPC) and enforced protein of Ψ synthase 10 (PUS10) recapitulates the phenotype of aged HSC, which is not achieved by its Ψ synthase activity. Consistently, we observed no difference of transcribed RNA pseudouridylation profile between young and aged HSPC. No significant alteration of hematopoietic homeostasis and HSC function is observed in young Pus10-/- mice, while aged Pus10-/- mice exhibit mild alteration of hematopoietic homeostasis and HSC function. Moreover, we observed that PUS10 is ubiquitinated by E3 ubiquitin ligase CRL4DCAF1 complex and the increase of PUS10 in aged HSPC is due to aging-declined CRL4DCAF1- mediated ubiquitination degradation signaling. Taken together, this study for the first time evaluated the role of PUS10 in HSC aging and function, and provided a novel insight into HSC rejuvenation and its clinical application.Aged hematopoietic stem cells (HSC) exhibit compromised reconstitution capacity and differentiation-bias towards myeloid lineage, however, the molecular mechanism behind it remains not fully understood. In this study, we observed that the expression of pseudouridine (Ψ) synthase 10 is increased in aged hematopoietic stem and progenitor cells (HSPC) and enforced protein of Ψ synthase 10 (PUS10) recapitulates the phenotype of aged HSC, which is not achieved by its Ψ synthase activity. Consistently, we observed no difference of transcribed RNA pseudouridylation profile between young and aged HSPC. No significant alteration of hematopoietic homeostasis and HSC function is observed in young Pus10-/- mice, while aged Pus10-/- mice exhibit mild alteration of hematopoietic homeostasis and HSC function. Moreover, we observed that PUS10 is ubiquitinated by E3 ubiquitin ligase CRL4DCAF1 complex and the increase of PUS10 in aged HSPC is due to aging-declined CRL4DCAF1- mediated ubiquitination degradation signaling. Taken together, this study for the first time evaluated the role of PUS10 in HSC aging and function, and provided a novel insight into HSC rejuvenation and its clinical application. Aged hematopoietic stem cells (HSC) exhibit compromised reconstitution capacity and differentiation-bias towards myeloid lineage, however, the molecular mechanism behind it remains not fully understood. In this study, we observed that the expression of pseudouridine (Ψ) synthase 10 is increased in aged hematopoietic stem and progenitor cells (HSPC) and enforced protein of Ψ synthase 10 (PUS10) recapitulates the phenotype of aged HSC, which is not achieved by its Ψ synthase activity. Consistently, we observed no difference of transcribed RNA pseudouridylation profile between young and aged HSPC. No significant alteration of hematopoietic homeostasis and HSC function is observed in young Pus10 -/- mice, while aged Pus10 -/- mice exhibit mild alteration of hematopoietic homeostasis and HSC function. Moreover, we observed that PUS10 is ubiquitinated by E3 ubiquitin ligase CRL4 DCAF1 complex and the increase of PUS10 in aged HSPC is due to aging-declined CRL4 DCAF1 -mediated ubiquitination degradation signaling. Taken together, this study for the first time evaluated the role of PUS10 in HSC aging and function, and provided a novel insight into HSC rejuvenation and its clinical application. |
| Author | Chen, Yunan Wang, Yuqian Shi, Minglei He, Hanqing Yi, Chengqi Zhang, Xinxiang Wang, Jianwei Cui, Yang Song, Jinghui Zhuang, Yuan Zhang, Zhenzhen Zhang, Xiaoting Zhang, Michael Q. Li, Mo |
| AuthorAffiliation | 6 Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital , Beijing, China 2 School of Medicine, Tsinghua University , Beijing, China 8 Department of Biological Sciences, Center for Systems Biology, the University of Texas , Richardson, TX, USA 1 School of Pharmaceutical Sciences, Tsinghua University , Beijing, China 5 Department of Basic Medical Sciences, School of Medicine, Institute for Immunology , Beijing Key Laboratory for Immunological Research on Chronic Diseases , THU-PKU Center for Life Sciences, Tsinghua University , Beijing, China 4 Beijing National Laboratory for Molecular Sciences, Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education, College of Chemistry and Molecular Engineering, Peking University , Beijing, China 7 MOE Key Laboratory of Bioinformatics; Division and Center for Synthetic & Systems Biology , BNRist, Department of Automation, Tsinghua University , Beijing, China 3 Department |
| AuthorAffiliation_xml | – name: 3 Department of Bioengineering, University of California San Diego , La Jolla, CA, USA – name: 2 School of Medicine, Tsinghua University , Beijing, China – name: 7 MOE Key Laboratory of Bioinformatics; Division and Center for Synthetic & Systems Biology , BNRist, Department of Automation, Tsinghua University , Beijing, China – name: 1 School of Pharmaceutical Sciences, Tsinghua University , Beijing, China – name: 6 Center for Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital , Beijing, China – name: 5 Department of Basic Medical Sciences, School of Medicine, Institute for Immunology , Beijing Key Laboratory for Immunological Research on Chronic Diseases , THU-PKU Center for Life Sciences, Tsinghua University , Beijing, China – name: 8 Department of Biological Sciences, Center for Systems Biology, the University of Texas , Richardson, TX, USA – name: 4 Beijing National Laboratory for Molecular Sciences, Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education, College of Chemistry and Molecular Engineering, Peking University , Beijing, China |
| Author_xml | – sequence: 1 givenname: Yuqian surname: Wang fullname: Wang, Yuqian – sequence: 2 givenname: Zhenzhen surname: Zhang fullname: Zhang, Zhenzhen – sequence: 3 givenname: Hanqing surname: He fullname: He, Hanqing – sequence: 4 givenname: Jinghui surname: Song fullname: Song, Jinghui – sequence: 5 givenname: Yang surname: Cui fullname: Cui, Yang – sequence: 6 givenname: Yunan surname: Chen fullname: Chen, Yunan – sequence: 7 givenname: Yuan surname: Zhuang fullname: Zhuang, Yuan – sequence: 8 givenname: Xiaoting surname: Zhang fullname: Zhang, Xiaoting – sequence: 9 givenname: Mo surname: Li fullname: Li, Mo – sequence: 10 givenname: Xinxiang surname: Zhang fullname: Zhang, Xinxiang – sequence: 11 givenname: Michael Q. surname: Zhang fullname: Zhang, Michael Q. – sequence: 12 givenname: Minglei surname: Shi fullname: Shi, Minglei – sequence: 13 givenname: Chengqi surname: Yi fullname: Yi, Chengqi – sequence: 14 givenname: Jianwei surname: Wang fullname: Wang, Jianwei |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 JW and CY developed the concept. JW and CY developed the methodology. YW, ZZ, HH, JS, YC, YC, YZ and XZ carried out the investigation. JW, CY, MS, MQZ, XZ and ML performed the formal analysis. JW, CY, MS and MQZ provided resources. JW and CY wrote the manuscript. JW and CY acquired funding. JW, CY, MS and MQZ supervised the study. Disclosures Contributions The data are available on request. All sequencing raw data were deposited in the National Center for Biotechnology Information Gene Expression Omnibus. The accession code is GSE213422 with the enter token atstusiqpxmhvmj. No conflicts of interest to disclose. Data-sharing statement |
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| Title | Aging-induced pseudouridine synthase 10 impairs hematopoietic stem cells |
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