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Developmental anomalies and neoplasia in animals and cells deficient in the large zinc finger protein KRC

Carl E Allen1, Natarajan Muthusamy, Steven E Weisbrode

  • 1Program of Molecular, Cellular, and Developmental Biology, College of Medicine and Public Health, The Ohio State University, Columbus, Ohio, USA.

Genes, Chromosomes & Cancer
|October 16, 2002
PubMed

Insights

The zinc finger protein KRC is not essential for V(D)J recombination but may regulate T-lymphocyte survival. KRC deficiency leads to growth anomalies and teratomas, suggesting KRC is a potential tumor suppressor gene.

Area of Science:

  • Molecular Biology
  • Immunology
  • Developmental Biology

Background:

  • The large zinc finger protein KRC interacts with V(D)J recombination signal sequences and the kappaB motif.
  • Disrupting KRC expression in cell lines increases proliferation and disrupts cell division.

Purpose of the Study:

  • To investigate the in vivo function of KRC using a RAG2-deficient blastocyst complementation model.
  • To determine KRC's role in V(D)J recombination, T-lymphocyte development, and tumor suppression.

Main Methods:

  • Generated KRC-deficient embryonic stem cells via homologous recombination.
  • Created KRC(-/-);RAG2(-/-) chimeric mice by blastocyst complementation.
  • Analyzed lymphoid compartments and tumor development in chimeric mice.

Main Results:

  • KRC is not essential for V(D)J recombination or early lymphoid development.
  • KRC-deficient chimeras showed a deficit in CD4(+)CD8(+) thymocytes at 6 months, indicating a role in T-lymphocyte survival.
  • One chimera developed a malignant teratoma derived from KRC-deficient cells, and immortalized KRC-deficient cell lines were established.

Conclusions:

  • KRC plays a role in T-lymphocyte survival.
  • KRC deficiency is associated with growth anomalies and neoplasia, suggesting KRC functions as a tumor suppressor gene.

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