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Structure of the murine c-sis proto-oncogene (Sis, PDGFB) encoding the B chain of platelet-derived growth factor

D T Bonthron1, P Sultan, T Collins

  • 1Human Genetics Unit, Edinburgh University, Department of Medicine, Western General Hospital, Scotland.

Genomics
|May 1, 1991
PubMed

Insights

The murine proto-oncogene c-sis (Sis), encoding platelet-derived growth factor B (PDGFB), was cloned. Its conserved structure and a unique exon suggest important regulatory roles in cell growth.

Area of Science:

  • Molecular biology
  • Oncogenes
  • Gene structure and regulation

Background:

  • The c-sis proto-oncogene encodes the B chain of platelet-derived growth factor (PDGF).
  • Understanding the structure of c-sis in different species aids in comprehending its role in cell growth and oncogenesis.

Purpose of the Study:

  • To clone and characterize the murine proto-oncogene c-sis (Sis, PDGFB).
  • To compare the structure of murine c-sis with its human and feline homologs.
  • To investigate potential regulatory elements within the c-sis gene.

Main Methods:

  • Gene cloning techniques were employed to isolate the murine c-sis proto-oncogene.
  • Sequence analysis was performed to determine the structural features and homology with other species.
  • Comparative analysis of exon-intron structure and noncoding regions was conducted.

Main Results:

  • The murine c-sis gene, encoding platelet-derived growth factor B (PDGFB), was successfully cloned.
  • Murine c-sis exhibits a seven-exon structure spanning approximately 20 kb, similar to human and feline homologs.
  • The predicted amino acid sequence of murine PDGF-B shows 89% identity to human PDGF-B.
  • A conserved noncoding region in exon 7, absent in v-sis, was identified across species.

Conclusions:

  • The structural similarity of murine c-sis to its homologs highlights conserved functions.
  • The conserved noncoding region in exon 7 may play a crucial role in regulating c-sis expression.
  • This finding provides insights into the oncogenic potential of the v-sis gene through alternative splicing.

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