Loss of Ribosomal Protein Paralog Rpl22-like1 Blocks Lymphoid Development without Affecting Protein Synthesis.


Journal

Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R

Informations de publication

Date de publication:
15 02 2022
Historique:
received: 06 07 2021
accepted: 30 11 2021
pubmed: 21 1 2022
medline: 22 2 2022
entrez: 20 1 2022
Statut: ppublish

Résumé

Ribosomal proteins are thought to primarily facilitate biogenesis of the ribosome and its ability to synthesize protein. However, in this study, we show that Rpl22-like1 (Rpl22l1) regulates hematopoiesis without affecting ribosome biogenesis or bulk protein synthesis. Conditional loss of murine Rpl22l1 using stage or lineage-restricted Cre drivers impairs development of several hematopoietic lineages. Specifically, Tie2-Cre-mediated ablation of Rpl22l1 in hemogenic endothelium impairs the emergence of embryonic hematopoietic stem cells. Ablation of Rpl22l1 in late fetal liver progenitors impairs the development of B lineage progenitors at the pre-B stage and development of T cells at the CD44

Identifiants

pubmed: 35046107
pii: jimmunol.2100668
doi: 10.4049/jimmunol.2100668
pmc: PMC8827804
mid: NIHMS1762258
doi:

Substances chimiques

RPL22L1 protein, mouse 0
Ribosomal Proteins 0
Tumor Suppressor Protein p53 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

870-880

Subventions

Organisme : NIAID NIH HHS
ID : P01 AI102853
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA006927
Pays : United States
Organisme : NIAID NIH HHS
ID : R37 AI110985
Pays : United States

Informations de copyright

Copyright © 2022 by The American Association of Immunologists, Inc.

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Auteurs

Shawn P Fahl (SP)

Blood Cell Development and Function Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111; and.

Robert Sertori (R)

Blood Cell Development and Function Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111; and.

Yong Zhang (Y)

Blood Cell Development and Function Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111; and.

Alejandra V Contreras (AV)

Blood Cell Development and Function Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111; and.

Bryan Harris (B)

Blood Cell Development and Function Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111; and.

Minshi Wang (M)

Blood Cell Development and Function Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111; and.

Jacqueline Perrigoue (J)

Blood Cell Development and Function Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111; and.

Siddharth Balachandran (S)

Blood Cell Development and Function Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111; and.

Brian K Kennedy (BK)

Departments of Biochemistry and Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.

David L Wiest (DL)

Blood Cell Development and Function Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111; and david.wiest@fccc.edu.

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