The Functional Significance of Absence: The Chromosomal Segment Harboring Tp53 Is Absent from the T55 Rat Radiation Hybrid Mapping PanelShow others and affiliations
2002 (English)In: Genomics, ISSN 0888-7543, E-ISSN 1089-8646, Vol. 79, no 6, p. 844-848Article in journal (Refereed) Published
Abstract [en]
The T55 rat radiation hybrid (RH) mapping panel has been reported to retain the entire rat genome at retention frequencies between 22% and 37%. However, we found that a small segment of rat chromosome 10 harboring at least four different genes, including Tp53, was completely absent from the panel (retention frequency = 0%). Two other markers located in the vicinity exhibited much reduced retention (2–6%). RH clones are generated by transferring highly fragmented DNA into a recipient cell. There might be a strong selection against the transfer and retention of chromosome segments harboring an intact Tp53, as the action of this gene might prevent proliferation and establishment of the RH clone. Our finding further suggests that unexpected low retention or absence of chromosome segments in an RH panel may represent indications that the segments harbor genes with important functions in cell proliferation control.
Place, publisher, year, edition, pages
Elsevier, 2002. Vol. 79, no 6, p. 844-848
Keywords [en]
Tp53, T55 panel, rat, radiation hybrid mapping, functional analysis
National Category
Genetics
Identifiers
URN: urn:nbn:se:his:diva-23013DOI: 10.1006/geno.2002.6785ISI: 000175963600015PubMedID: 12036299Scopus ID: 2-s2.0-0036275809OAI: oai:DiVA.org:his-23013DiVA, id: diva2:1781543
Funder
Wallenberg FoundationsErik Philip-Sörensens stiftelseCarl Tryggers foundation IngaBritt and Arne Lundberg’s Research FoundationThe Royal Swedish Academy of SciencesWilhelm och Martina Lundgrens Vetenskapsfond
Note
We thank Khalil Helou (Department of Oncology, Sahlgrenska Hospital, Göteborg, Sweden) for valuable remarks on FISH results. The D10Ncc3 marker plasmid was kindly provided by Toshikazu Ushijima (National Cancer Center Research Institute, Tokyo, Japan). This work was supported by grants from the Swedish Medical Research Council, the Wallenberg Foundation, the Erik Philip-Sörensen Foundation, the Carl Trygger Foundation, the IngaBritt and Arne Lundberg Research Foundation, the Royal Swedish Academy of Sciences, the Wilhelm and Martina Lundgren Foundation, and the Royal and Hvitfeldtska Foundation.
2023-07-102023-07-102023-07-10Bibliographically approved