ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Developmental arrest of T cells in Rpl22-deficient mice is dependent upon multiple p53 effectors.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Ribosomal protein control of hematopoietic stem cell transformation through regulation of metabolism.Cell reports · 2025Article
- Inhibition of Ribosome Biogenesis In Vivo Causes p53-Dependent Death and p53-Independent Dysfunction.Cellular and molecular gastroenterology and hepatology · 2025Article
- Article
- Loss of Ribosomal Protein Paralog Rpl22-like1 Blocks Lymphoid Development without Affecting Protein Synthesis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Puma- and Caspase9-mediated apoptosis is dispensable for p53-driven neural crest-based developmental defects.Cell death and differentiation · 2021Article
- Review
- Article
- Comparative transcriptomic analysis of skeletal muscle tissue during prenatal stages in Tongcheng and Yorkshire pig using RNA-seq.Functional & integrative genomics · 2018Article
- Translating the Game: Ribosomes as Active Players.Frontiers in genetics · 2018Review
- Rpl22 Loss Selectively Impairs αβ T Cell Development by Dysregulating Endoplasmic Reticulum Stress Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Ribosomal Protein Rpl22 Controls the Dissemination of T-cell Lymphoma.Cancer research · 2016Article
- RP-MDM2-p53 Pathway: Linking Ribosomal Biogenesis and Tumor Surveillance.Trends in cancer · 2016Review
- Splicing-Mediated Autoregulation Modulates Rpl22p Expression in Saccharomyces cerevisiae.PLoS genetics · 2016Article
- Role of ribosomal protein mutations in tumor development (Review).International journal of oncology · 2016Review
- Rpl22 is required for IME1 mRNA translation and meiotic induction in S. cerevisiae.Cell division · 2016Article
- Ribosome biogenesis dysfunction leads to p53-mediated apoptosis and goblet cell differentiation of mouse intestinal stem/progenitor cells.Cell death and differentiation · 2015Article
- Transcription factors and target genes of pre-TCR signaling.Cellular and molecular life sciences : CMLS · 2015Review
- Ribosomal proteins and human diseases: pathogenesis, molecular mechanisms, and therapeutic implications.Medicinal research reviews · 2015Review
- Regulatory Roles of Rpl22 in Hematopoiesis: An Old Dog with New Tricks.Critical reviews in immunology · 2015Review
- Rpl22 Loss Impairs the Development of B Lymphocytes by Activating a p53-Dependent Checkpoint.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
αβ and γδ lineage T cells are thought to arise from a common CD4(-)CD8(-) progenitor in the thymus. However, the molecular pathways controlling fate selection and maturation of these two lineages remain poorly understood. We demonstrated recently that a ubiquitously expressed ribosomal protein, Rpl22, is selectively required for the development of αβ lineage T cells. Germline ablation of Rpl22 impairs development of αβ lineage, but not γδ lineage, T cells through activation of a p53-dependent checkpoint. In this study, we investigate the downstream effectors used by p53 to impair T cell development. We found that many p53 targets were induced in Rpl22(-/-) thymocytes, including miR-34a, PUMA, p21(waf), Bax, and Noxa. Notably, the proapoptotic factor Bim, while not a direct p53 target, was also strongly induced in Rpl22(-/-) T cells. Gain-of-function analysis indicated that overexpression of miR-34a caused a developmental arrest reminiscent of that induced by p53 in Rpl22-deficient T cells; however, only a few p53 targets alleviated developmental arrest when individually ablated by gene targeting or knockdown. Co-elimination of PUMA and Bim resulted in a nearly complete restoration of development of Rpl22(-/-) thymocytes, indicating that p53-mediated arrest is enforced principally through effects on cell survival. Surprisingly, co-elimination of the primary p53 regulators of cell cycle arrest (p21(waf)) and apoptosis (PUMA) actually abrogated the partial rescue caused by loss of PUMA alone, suggesting that the G1 checkpoint protein p21(waf) facilitates thymocyte development in some contexts.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.