Jamie Russell

The University of Texas Southwestern Medical Center

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Bruce Beutler

The University of Texas Southwestern Medical Center

Jianhui Wang

The University of Texas Southwestern Medical Center

D. Gale Johnson

Mayo Clinic Hospital

Hexin Shi

The University of Texas Southwestern Medical Center

Subarna Ghosh

Serampore College

Dawei Wang

Lawrence Berkeley National Laboratory

Miao Tang

The University of Texas Southwestern Medical Center

Evan Nair‐Gill

The University of Texas Southwestern Medical Center

Aijie Liu

The University of Texas Southwestern Medical Center

Xue Zhong

The University of Texas Southwestern Medical Center

Cooperative Institutions

The University of Texas Southwestern Medical Center

Southwestern Medical Center

University of Tsukuba

Tsukuba International University

The University of Tokyo

Kansai Medical University

Kanazawa University

Chinese Academy of Sciences

Howard Hughes Medical Institute

The University of Texas MD Anderson Cancer Center

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Lrp10 suppresses IL7R limiting CD8 T cell homeostatic expansion and anti-tumor immunity

EMBO Reports (2024)

Jamie Russell Luming Chen Aijie Liu Jianhui Wang Subarna Ghosh

Abstract Signals emanating from the T-cell receptor (TCR), co-stimulatory receptors, and cytokine receptors each influence CD8 T-cell fate. Understanding how these signals respond to homeostatic and microenvironmental cues can reveal new ways to therapeutically direct T-cell function. Through forward genetic screening in mice, we discover that loss-of-function mutations in LDL receptor-related protein 10 ( Lrp10 ) cause naive and central memory CD8 T cells to accumulate in peripheral lymphoid organs. Lrp10 encodes a conserved cell surface protein of unknown immunological function. T-cell activation induces Lrp10 expression, which post-translationally suppresses IL7 receptor (IL7R) levels. Accordingly, Lrp10 deletion enhances T-cell homeostatic expansion through IL7R signaling. Lrp10 -deficient mice are also intrinsically resistant to syngeneic tumors. This phenotype depends on dense tumor infiltration of CD8 T cells, which display increased memory cell characteristics, reduced terminal exhaustion, and augmented responses to immune checkpoint inhibition. Here, we present Lrp10 as a new negative regulator of CD8 T-cell homeostasis and a host factor that controls tumor resistance with implications for immunotherapy.

Interleukin-7 receptor

Homeostasis

10.1038/s44319-024-00191-w

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Citations (2)

E2F1 suppresses skin carcinogenesis via the ARF-p53 pathway

Oncogene (2005)

Jamie Russell Regina L. Weaks Thomas R. Berton D. Gale Johnson

E2F1

10.1038/sj.onc.1209120

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Citations (15)

E2F4 and E2F1 Have Similar Proliferative Properties but Different Apoptotic and Oncogenic Properties In Vivo

Molecular and Cellular Biology (2000)

Dawei Wang Jamie Russell D. Gale Johnson

Loss of retinoblastoma (Rb) tumor suppressor function, as occurs in many cancers, leads to uncontrolled proliferation, an increased propensity to undergo apoptosis, and tumorigenesis. Rb negatively regulates multiple E2F transcription factors, but the role of the different E2F family members in manifesting the cellular response to Rb inactivation is unclear. To study the effect of deregulated E2F4 activity on cell growth control and tumorigenesis, transgenic mouse lines expressing the E2F4 gene under the control of a keratin 5 (K5) promoter were developed, and their phenotypes were compared to those of previously generated K5 E2F1 transgenic mice. In contrast to what has been observed in vitro, ectopically expressed E2F4 was found to localize to the nucleus and induce proliferation to an extent similar to that induced by E2F1 in transgenic tissue. Unlike E2F1, E2F4 does not induce apoptosis, and this correlates with the differential abilities of these two E2F species to stimulatep19ARF expression in vivo. To examine the role of E2F4 in tumor development, the mouse skin two-stage carcinogenesis model was utilized. Unlike E2F1 transgenic mice, E2F4 transgenic mice developed skin tumors with a decreased latency and increased incidence compared to those characteristics in wild-type controls. These findings demonstrate that while the effects of E2F1 and E2F4 on cell proliferation in vivo are similar, their apoptotic and oncogenic properties are quite different.

E2F1

E2F

Retinoblastoma protein

10.1128/.20.10.3417-3424.2000

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Citations (4)

Lrp10 suppresses IL7R limiting CD8 T cell homeostatic expansion and anti-tumor immunity

bioRxiv (Cold Spring Harbor Laboratory) (2023)

Jamie Russell Luming Chen Aijie Liu Jianhui Wang Subarna Ghosh

SUMMARY Signals emanating from the T cell receptor (TCR), co-stimulatory receptors, and cytokine receptors each influence CD8 T cell fate. Understanding how these signals respond to homeostatic and microenvironmental cues can reveal new ways to therapeutically direct T cell function. Through forward genetic screening in mice, we discovered that loss-of-function mutations in LDL receptor related protein 10 ( Lrp10 ) caused naïve and central memory CD8 T cells to accumulate in peripheral lymphoid organs. Lrp10 encodes a conserved cell surface protein of unknown immunological function. Lrp10 was induced with T cell activation and its expression post-translationally suppressed IL7 receptor (IL7R) levels. Accordingly, Lrp10 deletion enhanced T cell homeostatic expansion through IL7R signaling. Lrp10 -deficient mice were also intrinsically resistant to syngeneic tumors. This phenotype depended on dense tumor infiltration of CD8 T cells that displayed increased memory cell characteristics, reduced terminal exhaustion, and augmented responses to immune checkpoint inhibition. Here, we present Lrp10 as a new negative regulator of CD8 T cell homeostasis and a host factor that controls tumor resistance with implications for immunotherapy.

Interleukin-7 receptor

Limiting

Homeostasis

10.1101/2023.12.08.570738

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Characterization of E2F1's oncogenic, apoptotic and tumor-suppressive activities utilizing the K5 mouse model

Jamie Russell

E2F1

Source

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The class I myosin MYO1D binds to lipid and protects against colitis

Disease Models & Mechanisms (2018)

William McAlpine Kuan-wen Wang Jin Huk Choi Miguel San Miguel Sarah Grace McAlpine

ABSTRACT Myosin ID (MYO1D) is a member of the class I myosin family. We screened 48,649 third generation (G3) germline mutant mice derived from N-ethyl-N-nitrosourea-mutagenized grandsires for intestinal homeostasis abnormalities after oral administration of dextran sodium sulfate (DSS). We found and validated mutations in Myo1d as a cause of increased susceptibility to DSS-induced colitis. MYO1D is produced in the intestinal epithelium, and the colitis phenotype is dependent on the nonhematopoietic compartment of the mouse. Moreover, MYO1D appears to couple cytoskeletal elements to lipid in an ATP-dependent manner. These findings demonstrate that MYO1D is needed to maintain epithelial integrity and protect against DSS-induced colitis.

Intestinal epithelium

Brush border

Intestinal mucosa

10.1242/dmm.035923

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A viable hypomorphic Arnt2 mutation causes hyperphagic obesity, diabetes and hepatic steatosis

Disease Models & Mechanisms (2018)

Emre E. Turer Miguel San Miguel Kuan-wen Wang William McAlpine Feiya Ou

ABSTRACT Aryl hydrocarbon receptor nuclear translocator 2 (ARNT2) is a member of the basic helix-loop-helix/PER-ARNT-SIM (bHLH/PAS) transcription factor family. ARNT2 heterodimerizes with several members of the family, including single-minded homolog-1 (SIM1) and neuronal PAS domain protein 4 (NPAS4), primarily in neurons of the central nervous system. We screened 64,424 third-generation germline mutant mice derived from N-ethyl-N-nitrosourea (ENU)-mutagenized great-grandsires for weight abnormalities. Among 17 elevated body weight phenotypes identified and mapped, one strongly correlated with an induced missense mutation in Arnt2 using a semidominant model of inheritance. Causation was confirmed by CRISPR/Cas9 gene targeting to recapitulate the original ENU allele, specifying Arg74Cys (R74C). The CRISPR/Cas9-targeted (Arnt2R74C/R74C) mice demonstrated hyperphagia and increased adiposity as well as hepatic steatosis and abnormalities in glucose homeostasis. The mutant ARNT2 protein showed decreased transcriptional activity when coexpressed with SIM1. These findings establish a requirement for ARNT2-dependent genes in the maintenance of the homeostatic feeding response, necessary for prevention of obesity and obesity-related diseases.

Steatosis

10.1242/dmm.035451

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Citations (6)

Pain and rain

The New Scientist (2013)

Jamie Russell

10.1016/s0262-4079(13)61306-8

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Citations (0)

E2F4 and E2F1 Have Similar Proliferative Properties but Different Apoptotic and Oncogenic Properties In Vivo

Molecular and Cellular Biology (2000)

Dawei Wang Jamie Russell D. Gale Johnson

E2F1

E2F

Retinoblastoma protein

10.1128/mcb.20.10.3417-3424.2000

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Citations (89)

Large-scale forward genetics screening identifies Trpa1 as a chemosensor for predator odor-evoked innate fear behaviors

Nature Communications (2018)

Yibing Wang Liqin Cao Chia-Ying Lee Tomohiko Matsuo Kejia Wu

Innate behaviors are genetically encoded, but their underlying molecular mechanisms remain largely unknown. Predator odor 2,4,5-trimethyl-3-thiazoline (TMT) and its potent analog 2-methyl-2-thiazoline (2MT) are believed to activate specific odorant receptors to elicit innate fear/defensive behaviors in naive mice. Here, we conduct a large-scale recessive genetics screen of ethylnitrosourea (ENU)-mutagenized mice. We find that loss of Trpa1, a pungency/irritancy receptor, diminishes TMT/2MT and snake skin-evoked innate fear/defensive responses. Accordingly, Trpa1 -/- mice fail to effectively activate known fear/stress brain centers upon 2MT exposure, despite their apparent ability to smell and learn to fear 2MT. Moreover, Trpa1 acts as a chemosensor for 2MT/TMT and Trpa1-expressing trigeminal ganglion neurons contribute critically to 2MT-evoked freezing. Our results indicate that Trpa1-mediated nociception plays a crucial role in predator odor-evoked innate fear/defensive behaviors. The work establishes the first forward genetics screen to uncover the molecular mechanism of innate fear, a basic emotion and evolutionarily conserved survival mechanism.

10.1038/s41467-018-04324-3

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Citations (72)