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Cis-regulatory Sequences02:02

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Cis-regulatory sequences are short fragments of non-coding DNA that are present on the same chromosomes as the genes that they regulate. These fragments serve as binding sites for transcriptional regulators, proteins that are responsible for controlling gene transcription and differential gene expression across cell types in eukaryotes. Cis-regulatory sequences can be close to the gene of interest or thousands of bases away in the DNA sequence; however, those sequences that are further away are...
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Most plants use the C3 pathway for carbon fixation. However, some plants, such as sugar cane, corn, and cacti that grow in hot conditions, use alternative pathways to fix carbon and conserve energy loss due to photorespiration. Photorespiration is the process that occurs when the oxygen concentration is high. Under such conditions, the rubisco enzyme in the Calvin cycle binds O2 instead of CO2, which halts photosynthesis and consumes energy.
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Global regulatory systems in bacteria enable rapid and coordinated responses to environmental changes by integrating sensory inputs with gene expression, ensuring efficient adaptation to fluctuating conditions. Key global regulatory mechanisms include regulons, two-component systems, sigma factors, and secondary messengers.Regulons and Global RegulatorsA regulon is a collection of genes and operons controlled by a common global regulator. These regulators enable bacteria to prioritize resource...
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Related Experiment Video

Updated: Feb 7, 2026

DTI of the Visual Pathway - White Matter Tracts and Cerebral Lesions
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An IFNγ/CXCL2 regulatory pathway determines lesion localization during EAE.

Joshua S Stoolman1,2,3, Patrick C Duncker1,2, Amanda K Huber1

  • 1Holtom-Garrett Program in Neuroimmunology and Multiple Sclerosis Center, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI, 48109, USA.

Journal of Neuroinflammation
|July 18, 2018
PubMed
Summary

Interferon-gamma (IFNγ) regulates immune cell chemokine production, influencing where brain inflammation occurs in experimental autoimmune encephalomyelitis (EAE). Impaired IFNγ signaling leads to brainstem inflammation and ataxia, while intact signaling directs inflammation to the spinal cord.

Keywords:
ChemokinesCytokinesExperimental autoimmune encephalomyelitisInterferon-gammaMonocytesMultiple sclerosisNeutrophils

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Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE
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Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE

Published on: April 15, 2014

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Area of Science:

  • Neuroimmunology
  • Infectious Diseases
  • Immunology

Background:

  • T-helper 1 cells induce experimental autoimmune encephalomyelitis (EAE) with distinct clinical and pathological features depending on host genetics.
  • Myelin oligodendrocyte glycoprotein (MOG)-reactive Th1 cells cause ascending paralysis in wildtype (WT) mice and ataxia in IFNγ receptor (IFNγR)-deficient mice.
  • ELR+ CXC chemokines are crucial for atypical EAE (aEAE) but not conventional EAE (cEAE), yet their sources and regulation remain unclear.

Purpose of the Study:

  • To elucidate the cellular sources and localization of ELR+ CXC chemokines in the CNS during EAE.
  • To investigate the IFNγ-dependent pathways regulating chemokine production in the CNS.
  • To understand how these mechanisms dictate the distinct clinical phenotypes of EAE.

Main Methods:

  • Immunohistochemistry and in situ hybridization to map inflammatory lesions and chemokine distribution.
  • Flow cytometry and quantitative PCR (qPCR) to quantify chemokine and receptor levels on leukocyte subsets.
  • In vitro culture of neutrophils and macrophages to assess chemokine production under inflammatory stimuli.

Main Results:

  • Neutrophils, monocytes, and microglia are key sources of CXCL2 in the brainstem during aEAE.
  • IFNγ suppresses CXCL2 and CXCR2 transcription in myeloid cells and neutrophils, respectively, in WT mice.
  • This IFNγ-mediated suppression prevents brainstem infiltration and directs inflammation to the spinal cord in cEAE.

Conclusions:

  • An IFNγ-regulated CXCR2/CXCL2 feedback loop in innate immune cells dictates CNS infiltrate localization in Th1-mediated EAE.
  • Impaired IFNγ signaling increases CXCL2 production, leading to brainstem inflammation and ataxia.
  • IFNγ suppresses myeloid cell CXCL2 and CXCR2, promoting spinal cord inflammation and ascending paralysis, revealing a mechanism for distinct EAE presentations.