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Defects in lens fiber differentiation are linked to c-mos overexpression in transgenic mice

J S Khillan1, M K Oskarsson, F Propst

  • 1Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892.

Genes & Development
|December 1, 1987
PubMed

Insights

Transgenic mice with Moloney murine sarcoma virus LTR linked to c-mos developed severe eye abnormalities due to c-mos overexpression. Despite high transforming activity in cell lines, no tumors formed in the affected mouse lenses.

Area of Science:

  • Molecular Biology
  • Genetics
  • Developmental Biology

Background:

  • The c-mos proto-oncogene plays a critical role in cellular regulation.
  • Understanding the in vivo effects of c-mos overexpression is essential for developmental biology.

Purpose of the Study:

  • To investigate the effects of introducing a c-mos transgene into mice.
  • To analyze the consequences of c-mos overexpression on lens development and tumor formation.

Main Methods:

  • Generation of three transgenic mouse strains via embryo microinjection of a DNA construct containing the Moloney murine sarcoma virus LTR linked to murine c-mos.
  • Southern analysis of genomic DNA to determine transgene integration sites.
  • Histological examination of ocular tissues and RNA expression analysis.

Main Results:

  • Transgenic mice exhibited dominant changes in secondary lens fiber differentiation, leading to lens capsule breakdown and posterior protrusion.
  • Lens cells filled anterior and posterior chambers, with massive c-mos RNA overexpression specifically in the lens.
  • Despite the construct's transforming activity in NIH-3T3 cells, no hyperplasia or neoplasia were observed in the affected lenses.

Conclusions:

  • Overexpression of c-mos in the lens disrupts normal differentiation and leads to severe ocular abnormalities without inducing cancer.
  • The cellular environment of the lens may resist oncogenic transformation mediated by c-mos.

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