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Pombe checkpoint regulatory pathway. This checkpoint mediates cell growth arrest at G2/M when cells su¡ered DNA damage or replication block. FROM TRANSCRIPTION TO CELL CYCLE CHECKPOINT 23 FIG. 3. HDAC1 and hHus1 interact in vivo. Expression constructs for either the £agepitope tagged HDAC1 (HDAC1-£ag) or the HA-epitope tagged hHus1 (HA-hHus1) were transfected into COS-7 cells. Immunoprecipitation was carried out with anti-£ag antibody. The immunocomplexes were then examined by Western blot using anti-HA antibody.

The other is to study protein binding properties to discover new ligands and their function. The interpretation of data obtained by the combination of these techniques and also by DNA analysis requires powerful bioinformatic tools, such as MELANIE (Fig. 2) (Hochstrasser et al 1995, Wilkins et al 1996, 1997, 1998) and intranet access to non-redundant, curated and annotated databases (Bairoch & Apweiler 1997, Bairoch et al 1997, Hawkins et al 1999). We combined reproducible 2D PAGE techniques using narrow immobilized pH gradient (IPG) precasted gel strips, precasted mini SDS PAGE gels, a new digesting-transblot procedure PROTEOME COMPLEXITY 37 and direct MALDI scanning of a collecting PVDF membrane to display bacterial and human proteome sections (Hochstrasser 1998).

Half a dozen may therefore be required for each 30^ 40 kb just to de¢ne the haplotypes, and that's not including the actual causative mutations. At the level of mapping and trying to do discovery, one per gene, if it is the right kind, may be su¤cient. Most people would argue that more is better. Venter: Especially if you want to understand protein function. We spent a lot of e¡ort doing site-directed mutagenesis on seventransmembrane receptors to try to understand variation in each amino acid and how it relates to function, and so there's a pretty good data set on these receptors in terms of variation at each site and what is really functional.