Disease relevance of Dcc

• Phenotype of mice lacking functional Deleted in colorectal cancer (Dcc) gene [1].
• To determine whether the loss of alleles of Mcc and/or Dcc is necessary for the formation of intestinal adenomas, subchromosomal somatic events were induced by gamma-irradiation [2].

High impact information on Dcc

• Deleted in colorectal cancer (Dcc) is a receptor for netrin-1 that mediates its chemoattractive effect on commissural axons, but the signalling mechanisms that transduce this effect are poorly understood [3].
• Inactivation of the murine Dcc gene caused defects in axonal projections that are similar to those observed in netrin-1-deficient mice but did not affect growth, differentiation, morphogenesis or tumorigenesis in mouse intestine [1].
• Ventral migration of early-born neurons requires Dcc and is essential for the projections of primary afferents in the spinal cord [4].
• We examined LHRH neuron migration in Dcc-/- mice and found that trajectories of the cVNN and positions of LHRH neurons are abnormal [5].
• Potential candidate genes in this region include Smad4, Smad2, and Dcc [6].

Biological context of Dcc

• Last, interactions between the Dcc and Unc5h3 mutations were observed in gene dosage experiments [7].
• This chromosome carries both the Mcc and Dcc genes, which are homologs of genes that have been implicated in human colorectal cancer [2].

Anatomical context of Dcc

• In addition, we observe corticospinal tract defects in mice homozygous for a spontaneous mutation that truncates the Dcc transcript [7].

Other interactions of Dcc

• The netrin 1 receptors Unc5h3 and Dcc are necessary at multiple choice points for the guidance of corticospinal tract axons [7].

References