Stephen L. Madden

Analysis of human transcriptomes

nature genetics • volume 23 • december 1999 387 The term ‘synteny’ (or syntenic) refers to gene loci on the same chromosome regardless of whether or not they are genetically linked by classic linkage analysis1. This term was introduced in 1971 by John H. Renwick, of the London School of Hygiene and Tropical Medicine, at the 4th Internal Congress of Human Genetics in Paris with one of us (E.P.) in attendance. The need for such a term was suggested to J.H. Renwick by E.A. Murphy, of Johns Hopkins University2. It arose as a consequence of the new methods in gene mapping using somatic cell hybrid cells. Human genes located on the same chromosome with a genetic distance that could not be determined by the frequency of recombination lacked a term of reference. ‘Synteny’ means ‘same thread’ (or ribbon), a state of being together in location, as synchrony would be together in time. Although several textbooks3–10 and other reference works11–15 give a correct definition, the term synteny nowadays is often used to refer to gene loci in different organisms located on a chromosomal region of common evolutionary ancestry. This new usage of the term synteny does not correspond to its original definition and correct language derivation. A survey of 11 articles in Nature Genetics since 1992 using the term syntenic or synteny in either the title or the abstract revealed usage incorrect in 8 and ambiguous in 3. We believe molecular biologists ought to respect the original definition of synteny and its etymological derivation, especially as this term is still needed to refer to genes located on the same chromosome. We recognize the need to refer to gene loci of common ancestry. Correct terms exist: ‘paralogous’ for genes that arose from a common ancestor gene within one species and ‘orthologous’ for the same gene in different species. Eberhard Passarge1, Bernhard Horsthemke1 & Rosann A. Farber2 1Institut für Humangenetik, Universitätsklinikum Essen, Essen, Germany. 2Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. Correspondence should be addressed to E.P. (e-mail: eberhard.passarge@uni-essen.de).

SAGE transcript profiles for p53-dependent growth regulation.

Serial analysis of gene expression (SAGE) allows for a quantitative, representative, and comprehensive profile of gene expression. We have utilized SAGE technology to contrast the differential gene expression profile in rat embryo fibroblast cells producing temperature-sensitive p53 tumor suppressor protein at permissive or non-permissive temperatures. Analysis of ∼15 000 genes revealed that the expression of 14 genes (P<0.001, ⩾0.03% abundance) was dependent on functional p53 protein, whereas the expression of three genes was significantly higher in cells producing non-functional p53 protein. Those genes whose expression was increased by functional p53 include RAS, U6 snRNA, cyclin G, EGR-1, and several novel genes. The expression of actin, tubulin, and HSP70 genes was elevated at the non-permissive temperature for p53 function. Interestingly, the expression of several genes was dependent on a non-temperature-sensitive mutant p53 suggesting altered transcription profiles dependent on specific p53 mutant proteins. These results demonstrate the utility of SAGE for rapidly and reproducibly evaluating global transcriptional responses within different cell populations.