Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

Ablation of beta 1 integrin in mammary epithelium reveals a key role for integrin in glandular morphogenesis and differentiation

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Naylor, M. J.
  • Li, N.
  • Cheung, J.
  • Lowe, E. T.
  • Lambert, E.
  • Marlow, R.
  • Wang, P. B.
  • Schatzmann, F.
  • Wintermantel, T.
  • Schuetz, G.
  • Clarke, A. R.
  • Mueller, Ulrich
  • Hynes, N. E.
  • Streuli, C. H.

publication date

  • November 2005

journal

  • Journal of Cell Biology  Journal

abstract

  • Integrin-mediated adhesion regulates the development and function of a range of tissues; however, little is known about its role in glandular epithelium. To assess the contribution of beta1 integrin, we conditionally deleted its gene in luminal epithelia during different stages of mouse mammary gland development and in cultured primary mammary epithelia. Loss of beta1 integrin in vivo resulted in impaired alveologenesis and lactation. Cultured beta1 integrin-null cells displayed abnormal focal adhesion function and signal transduction and could not form or maintain polarized acini. In vivo, epithelial cells became detached from the extracellular matrix but remained associated with each other and did not undergo overt apoptosis. beta1 integrin-null mammary epithelial cells did not differentiate in response to prolactin stimulation because of defective Stat5 activation. In mice where beta1 integrin was deleted after the initiation of differentiation, fewer defects in alveolar morphology occurred, yet major deficiencies were also observed in milk protein and milk fat production and Stat5 activation, indicating a permissive role for beta1 integrins in prolactin signaling. This study demonstrates that beta1 integrin is critical for the alveolar morphogenesis of a glandular epithelium and for maintenance of its differentiated function. Moreover, it provides genetic evidence for the cooperation between integrin and cytokine signaling pathways.

subject areas

  • Animals
  • Antigens, CD29
  • Blotting, Western
  • Cell Adhesion
  • Cell Differentiation
  • Cells, Cultured
  • Crosses, Genetic
  • Cytokines
  • Epithelial Cells
  • Epithelium
  • Extracellular Signal-Regulated MAP Kinases
  • Gene Deletion
  • Gene Expression Regulation
  • Integrins
  • Lactation
  • Mammary Glands, Animal
  • Mice
  • Mice, Transgenic
  • Microscopy, Fluorescence
  • Models, Genetic
  • Prolactin
  • STAT5 Transcription Factor
  • Signal Transduction
  • Time Factors
scroll to property group menus

Identity

PubMed Central ID

  • PMC2171573

International Standard Serial Number (ISSN)

  • 0021-9525

Digital Object Identifier (DOI)

  • 10.1083/jcb.200503144

PubMed ID

  • 16301336
scroll to property group menus

Additional Document Info

start page

  • 717

end page

  • 728

volume

  • 171

issue

  • 4

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support