Information

Related Research Units

Infectious Diseases Research

Research Overview

The focus of our research program over the past several years has been the molecular genetic analysis of host-microbe interactions using Caenorhabditis elegans as a simple host organism in which to acquire a systems-level, molecular, cellular, and organismal view of how a simple animal host responds to pathogenic and commensal bacteria. Our studies have spanned evolutionarily conserved pathways of innate immunity, the integrative physiology that connects infection and immunity with cellular and organismal responses to stress, and how interactions with microbes influence neuronal signaling and behavior of C. elegans. We continue to bring a broad interdisciplinary perspective, experimentally grounded in the molecular genetics of C. elegans, to our current areas of research focus, including understanding how microbes and their secondary metabolites can modulate host neuroendocrine physiology and behavior.

 

Research Background

Dennis Kim received his MD and PhD degrees from Harvard Medical School, completed internship and residency at Brigham and Women’s Hospital, and clinical fellowship training in Infectious Diseases at the Brigham and Women’s Hospital and Massachusetts General Hospital. He completed postdoctoral research training in genetics at Massachusetts General Hospital. Prior to assuming his current position at Boston Children’s Hospital, for thirteen years he was a Professor in the Department of Biology at the Massachusetts Institute of Technology while maintaining clinical attending responsibilities in Infectious Diseases at the Massachusetts General Hospital.

 

Education

Medical School

Harvard Medical School
1997 Boston MA

Internship

Brigham & Women's Hospital
1998 Boston MA

Residency

Brigham & Women's Hospital
1999 Boston MA

Fellowship

Brigham & Women's Hospital/Massachusetts General Hospital
2003 Boston MA

Publications

  1. Bacteria are a major determinant of Orsay virus transmission and infection in Caenorhabditis elegans. Elife. 2024 Jul 11; 12. View Abstract
  2. Genetic variants that modify neuroendocrine gene expression and foraging behavior of C. elegans. Sci Adv. 2024 Jun 14; 10(24):eadk9481. View Abstract
  3. Bacteria Are a Major Determinant of Orsay Virus Transmission and Infection in Caenorhabditis elegans. bioRxiv. 2024 Mar 18. View Abstract
  4. Neuroendocrine gene expression coupling of interoceptive bacterial food cues to foraging behavior of C. elegans. Elife. 2024 Jan 17; 12. View Abstract
  5. Germline mitotic quiescence and cell death are induced in Caenorhabditis elegans by exposure to pathogenic Pseudomonas aeruginosa. Genetics. 2024 01 03; 226(1). View Abstract
  6. Neuroendocrine Gene Expression Coupling of Interoceptive Bacterial Food Cues to Foraging Behavior of C. elegans. bioRxiv. 2023 Nov 13. View Abstract
  7. Genetic Variants That Modify the Neuroendocrine Regulation of Foraging Behavior in C. elegans. bioRxiv. 2023 Sep 19. View Abstract
  8. Germline mitotic quiescence and programmed cell death are induced in C. elegans by exposure to pathogenic P. aeruginosa. bioRxiv. 2023 Aug 11. View Abstract
  9. Neuronal KGB-1 JNK MAPK signaling regulates the dauer developmental decision in response to environmental stress in Caenorhabditis elegans. Genetics. 2022 Jan 04; 220(1). View Abstract
  10. Host-microbe interactions and the behavior of Caenorhabditis elegans. J Neurogenet. 2020 Sep-Dec; 34(3-4):500-509. View Abstract
  11. Immediate activation of chemosensory neuron gene expression by bacterial metabolites is selectively induced by distinct cyclic GMP-dependent pathways in Caenorhabditis elegans. PLoS Genet. 2020 08; 16(8):e1008505. View Abstract
  12. Population Density Modulates the Duration of Reproduction of C. elegans. Curr Biol. 2020 07 06; 30(13):2602-2607.e2. View Abstract
  13. Global transcriptional regulation of innate immunity by ATF-7 in C. elegans. PLoS Genet. 2019 02; 15(2):e1007830. View Abstract
  14. Bacterial Siderophores Promote Animal Host Iron Acquisition and Growth. Cell. 2018 10 04; 175(2):311-312. View Abstract
  15. Endoplasmic Reticulum Homeostasis Is Modulated by the Forkhead Transcription Factor FKH-9 During Infection of Caenorhabditis elegans. Genetics. 2018 12; 210(4):1329-1337. View Abstract
  16. Signaling in the innate immune response. WormBook. 2018 08 14; 2018:1-35. View Abstract
  17. PDF-1 neuropeptide signaling regulates sexually dimorphic gene expression in shared sensory neurons of C. elegans. Elife. 2018 07 19; 7. View Abstract
  18. Molecular Determinants of the Regulation of Development and Metabolism by Neuronal eIF2a Phosphorylation in Caenorhabditis elegans. Genetics. 2017 05; 206(1):251-263. View Abstract
  19. Sexually dimorphic control of gene expression in sensory neurons regulates decision-making behavior in C. elegans. Elife. 2017 01 24; 6. View Abstract
  20. Age-Dependent Neuroendocrine Signaling from Sensory Neurons Modulates the Effect of Dietary Restriction on Longevity of Caenorhabditis elegans. PLoS Genet. 2017 01; 13(1):e1006544. View Abstract
  21. Mutations in Nonessential eIF3k and eIF3l Genes Confer Lifespan Extension and Enhanced Resistance to ER Stress in Caenorhabditis elegans. PLoS Genet. 2016 09; 12(9):e1006326. View Abstract
  22. IRE1 Sulfenylation by Reactive Oxygen Species Coordinates Cellular Stress Signaling. Mol Cell. 2016 08 18; 63(4):541-542. View Abstract
  23. Inhibition of Lithium-Sensitive Phosphatase BPNT-1 Causes Selective Neuronal Dysfunction in C. elegans. Curr Biol. 2016 07 25; 26(14):1922-8. View Abstract
  24. Signal Transduction: A Different Kind of Toll Is in the BAG. Curr Biol. 2015 Aug 31; 25(17):R767-9. View Abstract
  25. Tissue expression pattern of PMK-2 p38 MAPK is established by the miR-58 family in C. elegans. PLoS Genet. 2015 Feb; 11(2):e1004997. View Abstract
  26. Chemosensation of bacterial secondary metabolites modulates neuroendocrine signaling and behavior of C. elegans. Cell. 2014 Oct 09; 159(2):267-80. View Abstract
  27. Behavioral avoidance of pathogenic bacteria by Caenorhabditis elegans. Trends Immunol. 2014 Oct; 35(10):465-70. View Abstract
  28. The unfolded protein response in a pair of sensory neurons promotes entry of C. elegans into dauer diapause. Curr Biol. 2013 Dec 16; 23(24):2540-5. View Abstract
  29. Bacteria and the aging and longevity of Caenorhabditis elegans. Annu Rev Genet. 2013; 47:233-46. View Abstract
  30. Physiological IRE-1-XBP-1 and PEK-1 signaling in Caenorhabditis elegans larval development and immunity. PLoS Genet. 2011 Nov; 7(11):e1002391. View Abstract
  31. Natural polymorphisms in C. elegans HECW-1 E3 ligase affect pathogen avoidance behaviour. Nature. 2011 Nov 16; 480(7378):525-9. View Abstract
  32. Caenorhabditis elegans NPR-1-mediated behaviors are suppressed in the presence of mucoid bacteria. Proc Natl Acad Sci U S A. 2011 Aug 02; 108(31):12887-92. View Abstract
  33. A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans. PLoS Genet. 2011 May; 7(5):e1002082. View Abstract
  34. Phosphorylation of the conserved transcription factor ATF-7 by PMK-1 p38 MAPK regulates innate immunity in Caenorhabditis elegans. PLoS Genet. 2010 Apr 01; 6(4):e1000892. View Abstract
  35. An essential role for XBP-1 in host protection against immune activation in C. elegans. Nature. 2010 Feb 25; 463(7284):1092-5. View Abstract
  36. Tissue-specific activities of an immune signaling module regulate physiological responses to pathogenic and nutritional bacteria in C. elegans. Cell Host Microbe. 2009 Oct 22; 6(4):321-30. View Abstract
  37. The G protein-coupled receptor FSHR-1 is required for the Caenorhabditis elegans innate immune response. Proc Natl Acad Sci U S A. 2009 Feb 24; 106(8):2782-7. View Abstract
  38. A polymorphism in npr-1 is a behavioral determinant of pathogen susceptibility in C. elegans. Science. 2009 Jan 16; 323(5912):382-4. View Abstract
  39. Studying host-pathogen interactions and innate immunity in Caenorhabditis elegans. Dis Model Mech. 2008 Nov-Dec; 1(4-5):205-8. View Abstract
  40. Transcriptional responses to pathogens in Caenorhabditis elegans. Curr Opin Microbiol. 2008 Jun; 11(3):251-6. View Abstract
  41. p38 MAPK regulates expression of immune response genes and contributes to longevity in C. elegans. PLoS Genet. 2006 Nov 10; 2(11):e183. View Abstract
  42. Evolutionary perspectives on innate immunity from the study of Caenorhabditis elegans. Curr Opin Immunol. 2005 Feb; 17(1):4-10. View Abstract
  43. Integration of Caenorhabditis elegans MAPK pathways mediating immunity and stress resistance by MEK-1 MAPK kinase and VHP-1 MAPK phosphatase. Proc Natl Acad Sci U S A. 2004 Jul 27; 101(30):10990-4. View Abstract
  44. The Caenorhabditis elegans MAPK phosphatase VHP-1 mediates a novel JNK-like signaling pathway in stress response. EMBO J. 2004 Jun 02; 23(11):2226-34. View Abstract
  45. Requirement for a conserved Toll/interleukin-1 resistance domain protein in the Caenorhabditis elegans immune response. Proc Natl Acad Sci U S A. 2004 Apr 27; 101(17):6593-8. View Abstract
  46. Long-lived C. elegans daf-2 mutants are resistant to bacterial pathogens. Science. 2003 Jun 20; 300(5627):1921. View Abstract
  47. A conserved p38 MAP kinase pathway in Caenorhabditis elegans innate immunity. Science. 2002 Jul 26; 297(5581):623-6. View Abstract

Contact Dennis Kim

Phone: 617-919-2900
Fax: 617-730-0254
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