Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Myeloid development is selectively disrupted in PU.1 null mice

K L Anderson1, K A Smith, K Conners

  • 1The Burnham Institute, La Jolla, CA, USA.

Blood
|June 20, 1998
PubMed
Summary

The transcription factor PU.1 is crucial for myeloid and B-cell development. PU.1 gene disruption impairs hematopoietic stem cell proliferation and myeloid progenitor function, impacting neutrophil and monocyte/macrophage development.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Computational design of highly signalling-active membrane receptors through solvent-mediated allosteric networks.

Nature chemistry·2025
Same author

Examining the long-term effects of traumatic brain injury on fear extinction in male rats.

Frontiers in behavioral neuroscience·2023
Same author

Correction: Image guidance system use amongst Canadian otolaryngologists: a nationwide survey.

Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale·2022
Same author

Image guidance system use amongst Canadian otolaryngologists: a nationwide survey.

Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale·2022
Same author

CSO (Canadian Society of Otolaryngology - Head & Neck Surgery) position paper on return to Otolaryngology - Head & Neck Surgery Clinic Practice during the COVID-19 pandemic in Canada.

Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale·2020
Same author

A survey of ENT undergraduate teaching in the UK.

The Journal of laryngology and otology·2020

Area of Science:

  • Hematology
  • Molecular Biology
  • Immunology

Background:

  • The ets family transcription factor PU.1 is essential for the development of various hematopoietic cell lineages.
  • PU.1 expression is detected in monocytes/macrophages, neutrophils, mast cells, B cells, and early erythroblasts, but not in T cells.
  • Previous studies showed PU.1 gene disruption leads to absence of monocytes/macrophages and B cells, with retained T-cell development and impaired neutrophil development.

Purpose of the Study:

  • To investigate the functional consequences of PU.1 gene disruption on hematopoietic stem and progenitor cells.
  • To elucidate the role of PU.1 in myeloid cell proliferation and differentiation in response to specific growth factors.
  • To determine the impact of PU.1 deficiency on myeloid growth factor receptor expression and cell-autonomous effects.

Related Experiment Videos

Main Methods:

  • Analysis of PU.1 null hematopoietic cells' proliferation and colony formation in response to various cytokines (M-CSF, G-CSF, GM-CSF, IL-3).
  • Assessment of myeloid growth factor receptor expression (M-CSF, G-CSF, GM-CSF receptors) in PU.1 null cells.
  • Evaluation of myeloid progenitor colony size and cell type production (neutrophils, monocytes/macrophages) under specific cytokine conditions (IL-3, IL-6, SCF).

Main Results:

  • PU.1 null hematopoietic cells failed to proliferate or form colonies in response to M-CSF, G-CSF, and GM-CSF.
  • PU.1 null cells showed reduced proliferation in response to IL-3 and had minimal/undetectable expression of corresponding CSF receptors.
  • PU.1 null myeloid progenitors produced smaller colonies and generated neutrophils but not monocytes/macrophages, suggesting cell-autonomous effects beyond receptor alterations.

Conclusions:

  • PU.1 gene disruption profoundly affects hematopoietic stem and progenitor cell function, leading to impaired myeloid development.
  • The absence of PU.1 results in reduced myeloid expansion and altered neutrophil development, partly due to impaired receptor expression and cell-autonomous effects.
  • PU.1 is critical for regulating developmentally programmed hematopoietic processes essential for myeloid lineage commitment and expansion.