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Article ; Online: Reply to Chien: Clarification of the effect of ligand on γδ-TCR repertoire selection.

Fahl, Shawn P / Wiest, David L

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 16, Page(s) E3607–E3608

MeSH term(s)	Ligands ; Receptors, Antigen, T-Cell, gamma-delta
Chemical Substances	Ligands ; Receptors, Antigen, T-Cell, gamma-delta
Language	English
Publishing date	2018-04-03
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1804193115
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Article ; Online: c-Myb Coordinates Survival and the Expression of Genes That Are Critical for the Pre-BCR Checkpoint.

Fahl, Shawn P / Daamen, Andrea R / Crittenden, Rowena B / Bender, Timothy P

Journal of immunology (Baltimore, Md. : 1950)

2018 Volume 200, Issue 10, Page(s) 3450–3463

Abstract: The c-Myb transcription factor is required for adult hematopoiesis, yet little is known about c-Myb function during lineage-specific differentiation due to the embryonic lethality ... ...

Abstract	The c-Myb transcription factor is required for adult hematopoiesis, yet little is known about c-Myb function during lineage-specific differentiation due to the embryonic lethality of
MeSH term(s)	Animals ; Antigens, CD19/metabolism ; Cell Differentiation/physiology ; Cell Proliferation/physiology ; Cyclin D3/metabolism ; Mice ; Precursor Cells, B-Lymphoid/metabolism ; Proto-Oncogene Proteins c-myb/metabolism ; Receptors, CXCR4/metabolism ; Receptors, Interleukin-7/metabolism ; STAT5 Transcription Factor/metabolism ; Signal Transduction/physiology ; Suppressor of Cytokine Signaling 3 Protein/metabolism
Chemical Substances	Antigens, CD19 ; Cyclin D3 ; Proto-Oncogene Proteins c-myb ; Receptors, CXCR4 ; Receptors, Interleukin-7 ; STAT5 Transcription Factor ; Suppressor of Cytokine Signaling 3 Protein ; interleukin-7 receptor, alpha chain
Language	English
Publishing date	2018-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1302303
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Article ; Online: Loss of Ribosomal Protein Paralog Rpl22-like1 Blocks Lymphoid Development without Affecting Protein Synthesis.

Fahl, Shawn P / Sertori, Robert / Zhang, Yong / Contreras, Alejandra V / Harris, Bryan / Wang, Minshi / Perrigoue, Jacqueline / Balachandran, Siddharth / Kennedy, Brian K / Wiest, David L

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 208, Issue 4, Page(s) 870–880

Abstract: 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 ... ...

Abstract	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
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Cell Lineage/immunology ; Cell Plasticity/genetics ; Cell Plasticity/immunology ; Gene Expression Profiling ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Immunophenotyping ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Lymphopoiesis/genetics ; Mice ; Mice, Knockout ; Protein Biosynthesis ; Ribosomal Proteins/deficiency ; Spleen/cytology ; Spleen/immunology ; Spleen/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	RPL22L1 protein, mouse ; Ribosomal Proteins ; Tumor Suppressor Protein p53
Language	English
Publishing date	2022-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2100668
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Article: Ribosomal protein control of hematopoietic stem cell transformation through direct, non-canonical regulation of metabolism.

Harris, Bryan / Singh, Dinesh K / Verma, Monika / Fahl, Shawn P / Rhodes, Michele / Sprinkle, Shanna R / Wang, Minshi / Zhang, Yong / Perrigoue, Jaqueline / Kessel, Rachel / Peri, Suraj / West, Joshua / Giricz, Orsi / Boultwood, Jacqueline / Pellagatti, Andrea / Ramesh, K H / Montagna, Cristina / Pradhan, Kith / Tyner, Jeffrey W /

Kennedy, Brian K / Holinstat, Michael / Steidl, Ulrich / Sykes, Stephen / Verma, Amit / Wiest, David L

bioRxiv : the preprint server for biology

2023

Abstract: We report here that expression of the ribosomal protein, RPL22, is frequently reduced in human myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML); reduced RPL22 expression is associated with worse outcomes. Mice null for Rpl22 display ... ...

Abstract	We report here that expression of the ribosomal protein, RPL22, is frequently reduced in human myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML); reduced RPL22 expression is associated with worse outcomes. Mice null for Rpl22 display characteristics of an MDS-like syndrome and develop leukemia at an accelerated rate. Rpl22-deficient mice also display enhanced hematopoietic stem cell (HSC) self-renewal and obstructed differentiation potential, which arises not from reduced protein synthesis but from increased expression of the Rpl22 target, ALOX12, an upstream regulator of fatty acid oxidation (FAO). The increased FAO mediated by Rpl22-deficiency also persists in leukemia cells and promotes their survival. Altogether, these findings reveal that Rpl22 insufficiency enhances the leukemia potential of HSC via non-canonical de-repression of its target, ALOX12, which enhances FAO, a process that may serve as a therapeutic vulnerability of Rpl22 low MDS and AML leukemia cells. Highlights: RPL22 insufficiency is observed in MDS/AML and is associated with reduced survivalRpl22-deficiency produces an MDS-like syndrome and facilitates leukemogenesisRpl22-deficiency does not impair global protein synthesis by HSCRpl22 controls leukemia cell survival by non-canonical regulation of lipid oxidation
Language	English
Publishing date	2023-06-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.31.543132
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Article ; Online: The ERK2-DBP domain opposes pathogenesis of a mouse JAK2V617F-driven myeloproliferative neoplasm.

Zhang, Yong / Truong, Billy / Fahl, Shawn P / Martinez, Esteban / Cai, Kathy Q / Al-Saleem, Essel D / Gong, Yulan / Liebermann, Dan A / Soboloff, Jonathan / Dunbrack, Roland / Levine, Ross L / Fletcher, Steven / Kappes, Dietmar / Sykes, Stephen M / Shapiro, Paul / Wiest, David L

Blood

2022 Volume 140, Issue 4, Page(s) 359–373

Abstract: Although Ras/mitogen-activated protein kinase (MAPK) signaling is activated in most human cancers, attempts to target this pathway using kinase-active site inhibitors have not typically led to durable clinical benefit. To address this shortcoming, we ... ...

Abstract	Although Ras/mitogen-activated protein kinase (MAPK) signaling is activated in most human cancers, attempts to target this pathway using kinase-active site inhibitors have not typically led to durable clinical benefit. To address this shortcoming, we sought to test the feasibility of an alternative targeting strategy, focused on the ERK2 substrate binding domains, D and DEF binding pocket (DBP). Disabling the ERK2-DBP domain in mice caused baseline erythrocytosis. Consequently, we investigated the role of the ERK2-D and -DBP domains in disease, using a JAK2-dependent model of polycythemia vera (PV). Of note, inactivation of the ERK2-DBP domain promoted the progression of disease from PV to myelofibrosis, suggesting that the ERK2-DBP domain normally opposes progression. ERK2-DBP inactivation also prevented oncogenic JAK2 kinase (JAK2V617F) from promoting oncogene-induced senescence in vitro. The ERK2-DBP mutation attenuated JAK2-mediated oncogene-induced senescence by preventing the physical interaction of ERK2 with the transcription factor Egr1. Because inactivation of the ERK2-DBP created a functional ERK2 kinase limited to binding substrates through its D domain, these data suggested that the D domain substrates were responsible for promoting oncogene-induced progenitor growth and tumor progression and that pharmacologic targeting of the ERK2-D domain may attenuate cancer cell growth. Indeed, pharmacologic agents targeting the ERK2-D domain were effective in attenuating the growth of JAK2-dependent myeloproliferative neoplasm cell lines. Taken together, these data indicate that the ERK-D and -DBP domains can play distinct roles in the progression of neoplasms and that the D domain has the potential to be a potent therapeutic target in Ras/MAPK-dependent cancers.
MeSH term(s)	Animals ; Cell Line ; Humans ; Janus Kinase 2/genetics ; MAP Kinase Signaling System ; Mice ; Mitogen-Activated Protein Kinases ; Phosphorylation ; Polycythemia Vera ; Signal Transduction
Chemical Substances	Janus Kinase 2 (EC 2.7.10.2) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-04-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2021013068
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Article ; Online: The E protein-TCF1 axis controls γδ T cell development and effector fate.

Fahl, Shawn P / Contreras, Alejandra V / Verma, Anjali / Qiu, Xiang / Harly, Christelle / Radtke, Freddy / Zúñiga-Pflücker, Juan Carlos / Murre, Cornelis / Xue, Hai-Hui / Sen, Jyoti Misra / Wiest, David L

Cell reports

2021 Volume 34, Issue 5, Page(s) 108716

Abstract: TCF1 plays a critical role in T lineage commitment and the development of αβ lineage T cells, but its role in γδ T cell development remains poorly understood. Here, we reveal a regulatory axis where T cell receptor (TCR) signaling controls TCF1 ... ...

Abstract	TCF1 plays a critical role in T lineage commitment and the development of αβ lineage T cells, but its role in γδ T cell development remains poorly understood. Here, we reveal a regulatory axis where T cell receptor (TCR) signaling controls TCF1 expression through an E-protein-bound regulatory element in the Tcf7 locus, and this axis regulates both γδ T lineage commitment and effector fate. Indeed, the level of TCF1 expression plays an important role in setting the threshold for γδ T lineage commitment and modulates the ability of TCR signaling to influence effector fate adoption by γδ T lineage progenitors. This finding provides mechanistic insight into how TCR-mediated repression of E proteins promotes the development of γδ T cells and their adoption of the interleukin (IL)-17-producing effector fate. IL-17-producing γδ T cells have been implicated in cancer progression and in the pathogenesis of psoriasis and multiple sclerosis.
MeSH term(s)	Animals ; Cell Differentiation ; Hepatocyte Nuclear Factor 1-alpha/metabolism ; Humans ; Mice ; Models, Immunological ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Signal Transduction
Chemical Substances	Hepatocyte Nuclear Factor 1-alpha ; Hnf1a protein, mouse ; Receptors, Antigen, T-Cell, gamma-delta
Language	English
Publishing date	2021-01-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.108716
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Article ; Online: Origins of γδ T cell effector subsets: a riddle wrapped in an enigma.

Fahl, Shawn P / Coffey, Francis / Wiest, David L

Journal of immunology (Baltimore, Md. : 1950)

2014 Volume 193, Issue 9, Page(s) 4289–4294

Abstract: αβ and γδ T cells are thought to arise from a common precursor in the thymus but play distinct roles in pathogen resistance. Although conventional αβ T cells exit the thymus in a naive state and acquire effector function in the periphery, the effector ... ...

Abstract	αβ and γδ T cells are thought to arise from a common precursor in the thymus but play distinct roles in pathogen resistance. Although conventional αβ T cells exit the thymus in a naive state and acquire effector function in the periphery, the effector fate of many γδ T cells is specified in the thymus and exhibits limited plasticity thereafter. This review describes the current models that have been proposed to explain the acquisition of effector fate by γδ T cells, as well as the apparent linkage to Vγ gene usage. The two predominant models are the predetermination model, which suggests that effector fate is determined prior to TCR expression, perhaps in association with the developmental timing of Vγ rearrangement, and the TCR-dependence model, which proposes that the nature of the TCR signal, particularly its intensity or duration, plays an important role in influencing effector fate.
MeSH term(s)	Animals ; Cell Differentiation/physiology ; Humans ; Models, Immunological ; Receptors, Antigen, T-Cell, alpha-beta ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Signal Transduction ; T-Cell Antigen Receptor Specificity/immunology ; T-Lymphocyte Subsets/cytology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism
Chemical Substances	Receptors, Antigen, T-Cell, alpha-beta ; Receptors, Antigen, T-Cell, gamma-delta
Language	English
Publishing date	2014-10-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1401813
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Article: Regulatory Roles of Rpl22 in Hematopoiesis: An Old Dog with New Tricks.

Fahl, Shawn P / Wang, Minshi / Zhang, Yong / Duc, Anne-Cecile E / Wiest, David L

Critical reviews in immunology

2016 Volume 35, Issue 5, Page(s) 379–400

Abstract: Ribosomal proteins have long been known to serve critical roles in facilitating the biogenesis of the ribosome and its ability to synthesize proteins. However, evidence is emerging that suggests ribosomal proteins are also capable of performing tissue- ... ...

Abstract	Ribosomal proteins have long been known to serve critical roles in facilitating the biogenesis of the ribosome and its ability to synthesize proteins. However, evidence is emerging that suggests ribosomal proteins are also capable of performing tissue-restricted, regulatory functions that impact normal development and pathological conditions, including cancer. The challenge in studying such regulatory functions is that elimination of many ribosomal proteins also disrupts ribosome biogenesis and/or function. Thus, it is difficult to determine whether developmental abnormalities resulting from ablation of a ribosomal protein result from loss of core ribosome functions or from loss of the regulatory function of the ribosomal protein. Rpl22, a ribosomal protein component of the large 60S subunit, provides insight into this conundrum; Rpl22 is dispensable for both ribosome biogenesis and protein synthesis yet its ablation causes tissue-restricted disruptions in development. Here we review evidence supporting the regulatory functions of Rpl22 and other ribosomal proteins.
MeSH term(s)	Animals ; Dogs ; Embryonic Development ; Hematopoiesis ; Humans ; Organ Specificity ; RNA-Binding Proteins/immunology ; RNA-Binding Proteins/metabolism ; Ribosomal Proteins/immunology ; Ribosomal Proteins/metabolism ; Ribosomes/physiology
Chemical Substances	RNA-Binding Proteins ; Ribosomal Proteins ; RPL22 protein, human (135844-68-7)
Language	English
Publishing date	2016-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1353116-5
ISSN	1040-8401
ISSN	1040-8401
DOI	10.1615/critrevimmunol.v35.i5.30
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Article ; Online: Rpl22 Loss Impairs the Development of B Lymphocytes by Activating a p53-Dependent Checkpoint.

Fahl, Shawn P / Harris, Bryan / Coffey, Francis / Wiest, David L

Journal of immunology (Baltimore, Md. : 1950)

2014 Volume 194, Issue 1, Page(s) 200–209

Abstract: Although ribosomal proteins facilitate the ribosome’s core function of translation, emerging evidence suggests that some ribosomal proteins are also capable of performing tissue-restricted functions either from within specialized ribosomes or from ... ...

Abstract	Although ribosomal proteins facilitate the ribosome’s core function of translation, emerging evidence suggests that some ribosomal proteins are also capable of performing tissue-restricted functions either from within specialized ribosomes or from outside of the ribosome. In particular, we have previously demonstrated that germline ablation of the gene encoding ribosomal protein Rpl22 causes a selective and p53-dependent arrest of ab T cell progenitors at the b-selection checkpoint. We have now identified a crucial role for Rpl22 during early B cell development. Germline ablation of Rpl22 results in a reduction in the absolute number of B-lineage progenitors in the bone marrow beginning at the pro–B cell stage. Although Rpl22-deficient pro–B cells are hyporesponsive to IL-7, a key cytokine required for early B cell development, the arrest of B cell development does not result from disrupted IL-7 signaling. Instead, p53 induction appears to be responsible for the developmental defects, as Rpl22 deficiency causes increased expression of p53 and activation of downstream p53 target genes, and p53 deficiency rescues the defect in B cell development in Rpl22-deficient mice. Interestingly, the requirement for Rpl22 in the B cell lineage appears to be developmentally restricted, because Rpl22-deficient splenic B cells proliferate normally in response to Ag receptor and Toll receptor stimuli and undergo normal class-switch recombination. These results indicate that Rpl22 performs a critical, developmentally restricted role in supporting early B cell development by preventing p53 induction.
MeSH term(s)	Animals ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cell Differentiation/genetics ; Cell Proliferation/genetics ; Cells, Cultured ; Homeodomain Proteins/genetics ; Immunoglobulin Class Switching/immunology ; Interleukin-7/genetics ; Lymphocyte Activation/immunology ; Mice ; Mice, Knockout ; RNA-Binding Proteins/genetics ; Ribosomal Proteins/genetics ; Ribosomes/genetics ; Tumor Suppressor Protein p53/biosynthesis ; Tumor Suppressor Protein p53/genetics ; V(D)J Recombination/genetics ; V(D)J Recombination/immunology
Chemical Substances	Homeodomain Proteins ; Interleukin-7 ; RNA-Binding Proteins ; RPL22 protein, mouse ; Ribosomal Proteins ; Tumor Suppressor Protein p53 ; RAG-1 protein (128559-51-3)
Language	English
Publishing date	2014-11-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1402242
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Article ; Online: Role of a selecting ligand in shaping the murine γδ-TCR repertoire.

Fahl, Shawn P / Coffey, Francis / Kain, Lisa / Zarin, Payam / Dunbrack, Roland L / Teyton, Luc / Zúñiga-Pflücker, Juan Carlos / Kappes, Dietmar J / Wiest, David L

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 8, Page(s) 1889–1894

Abstract: Unlike αβ-T lineage cells, where the role of ligand in intrathymic selection is well established, the role of ligand in the development of γδ-T cells remains controversial. Here we provide evidence for the role of a bona fide selecting ligand in shaping ... ...

Abstract	Unlike αβ-T lineage cells, where the role of ligand in intrathymic selection is well established, the role of ligand in the development of γδ-T cells remains controversial. Here we provide evidence for the role of a bona fide selecting ligand in shaping the γδ-T cell-receptor (TCR) repertoire. Reactivity of the γδ-TCR with the major histocompatibility complex (MHC) Class Ib ligands, H2-T10/22, is critically dependent upon the EGYEL motif in the complementarity determining region 3 (CDR3) of TCRδ. In the absence of H2-T10/22 ligand, the commitment of H2-T10/22 reactive γδ-T cells to the γδ fate is diminished, and the specification of those γδ committed cells to the IFN-γ or interleukin-17 effector fate is altered. Furthermore, those cells that do adopt the γδ fate and mature exhibit a profound alteration in the γδTCR repertoire, including depletion of the EGYEL motif and reductions in both CDR3δ length and charge. Taken together, these data suggest that ligand plays an important role in shaping the TCR repertoire of γδ-T cells.
MeSH term(s)	Animals ; Cell Lineage ; Ligands ; Mice ; Protein Binding ; Receptors, Antigen, T-Cell, gamma-delta/genetics ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; T-Lymphocyte Subsets/physiology
Chemical Substances	Ligands ; Receptors, Antigen, T-Cell, gamma-delta
Language	English
Publishing date	2018-02-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1718328115
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