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ABI2-deficient mice exhibit defective cell migration, aberrant dendritic spine morphogenesis, and deficits in learning and memory.

Publication ,  Journal Article
Grove, M; Demyanenko, G; Echarri, A; Zipfel, PA; Quiroz, ME; Rodriguiz, RM; Playford, M; Martensen, SA; Robinson, MR; Wetsel, WC; Maness, PF ...
Published in: Mol Cell Biol
December 2004

The Abl-interactor (Abi) family of adaptor proteins has been linked to signaling pathways involving the Abl tyrosine kinases and the Rac GTPase. Abi proteins localize to sites of actin polymerization in protrusive membrane structures and regulate actin dynamics in vitro. Here we demonstrate that Abi2 modulates cell morphogenesis and migration in vivo. Homozygous deletion of murine abi2 produced abnormal phenotypes in the eye and brain, the tissues with the highest Abi2 expression. In the absence of Abi2, secondary lens fiber orientation and migration were defective in the eye, without detectable defects in proliferation, differentiation, or apoptosis. These phenotypes were consistent with the localization of Abi2 at adherens junctions in the developing lens and at nascent epithelial cell adherens junctions in vitro. Downregulation of Abi expression by RNA interference impaired adherens junction formation and correlated with downregulation of the Wave actin-nucleation promoting factor. Loss of Abi2 also resulted in cell migration defects in the neocortex and hippocampus, abnormal dendritic spine morphology and density, and severe deficits in short- and long-term memory. These findings support a role for Abi2 in the regulation of cytoskeletal dynamics at adherens junctions and dendritic spines, which is critical for intercellular connectivity, cell morphogenesis, and cognitive functions.

Duke Scholars

Published In

Mol Cell Biol

DOI

ISSN

0270-7306

Publication Date

December 2004

Volume

24

Issue

24

Start / End Page

10905 / 10922

Location

United States

Related Subject Headings

  • RNA, Small Interfering
  • RNA Interference
  • Neocortex
  • Morphogenesis
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice
  • Memory
  • Lens, Crystalline
  • Learning
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Grove, M., Demyanenko, G., Echarri, A., Zipfel, P. A., Quiroz, M. E., Rodriguiz, R. M., … Pendergast, A. M. (2004). ABI2-deficient mice exhibit defective cell migration, aberrant dendritic spine morphogenesis, and deficits in learning and memory. Mol Cell Biol, 24(24), 10905–10922. https://doi.org/10.1128/MCB.24.24.10905-10922.2004
Grove, Matthew, Galina Demyanenko, Asier Echarri, Patricia A. Zipfel, Marisol E. Quiroz, Ramona M. Rodriguiz, Martin Playford, et al. “ABI2-deficient mice exhibit defective cell migration, aberrant dendritic spine morphogenesis, and deficits in learning and memory.Mol Cell Biol 24, no. 24 (December 2004): 10905–22. https://doi.org/10.1128/MCB.24.24.10905-10922.2004.
Grove M, Demyanenko G, Echarri A, Zipfel PA, Quiroz ME, Rodriguiz RM, et al. ABI2-deficient mice exhibit defective cell migration, aberrant dendritic spine morphogenesis, and deficits in learning and memory. Mol Cell Biol. 2004 Dec;24(24):10905–22.
Grove, Matthew, et al. “ABI2-deficient mice exhibit defective cell migration, aberrant dendritic spine morphogenesis, and deficits in learning and memory.Mol Cell Biol, vol. 24, no. 24, Dec. 2004, pp. 10905–22. Pubmed, doi:10.1128/MCB.24.24.10905-10922.2004.
Grove M, Demyanenko G, Echarri A, Zipfel PA, Quiroz ME, Rodriguiz RM, Playford M, Martensen SA, Robinson MR, Wetsel WC, Maness PF, Pendergast AM. ABI2-deficient mice exhibit defective cell migration, aberrant dendritic spine morphogenesis, and deficits in learning and memory. Mol Cell Biol. 2004 Dec;24(24):10905–10922.

Published In

Mol Cell Biol

DOI

ISSN

0270-7306

Publication Date

December 2004

Volume

24

Issue

24

Start / End Page

10905 / 10922

Location

United States

Related Subject Headings

  • RNA, Small Interfering
  • RNA Interference
  • Neocortex
  • Morphogenesis
  • Mice, Knockout
  • Mice, Inbred C57BL
  • Mice
  • Memory
  • Lens, Crystalline
  • Learning