Technology

Scanning of guanine–guanine mismatches in DNA by synthetic ligands using surface plasmon resonance. Nakatani, K. et al. Nature Biotechnol. 19, 51–55 (2001) [Pubmed]

Scanning methods that will detect DNA sequence variations are in high demand and this paper presents a highly specific and sensitive way of detecting G·G mismatches without using labour-intensive gel-based techniques. A synthetic ligand that is specific for G·G mismatches is bound to a sensor chip. The DNA molecules that are captured by the chip change the reflective index of polarized light, thus revealing the presence of a G·G mismatch in a DNA sample.

Genomics

Functional annotation of a full-length mouse cDNA collection. The RIKEN Genome Exploration Research Group Phase II Team and the FANTOM Consortium. Nature, 409, 685–690 (2001) PubMed

The aim of the Mouse Gene Encyclopaedia Project is to identify and sequence every transcript encoded in the mouse genome by sequencing and annotating full-length cDNA clones, and mapping them onto the genome. They now report the characterization of the first 21,076 clones of the collection. The clones, which correspond to ∼13,000 unique genes, were functionally annotated according to their degree of relationship to known mouse or human genes, their metabolic function and the presence of protein motifs.

Disease model

A mouse model of multiple endocrine neoplasia, type 1, develops multiple endocrine tumors. Crabtree, J. S. et al. Proc. Natl Acad. Sci. USA 98, 1118–1123 (2001) [PubMed]

Multiple endocrine neoplasia type I (MEN1) is characterized mainly by tumours of the parathyroid, pancreas and anterior pituitary. The responsible gene, MEN1, is inherited as an autosomal dominant and behaves as a tumour-suppressor gene in humans. Somatic loss of the wild-type copy of MEN1 is seen in affected patients. A mouse knockout model of MEN1 was made using homologous recombination. Whereas homozygous Men1 mice die in utero , heterozygous mice recapitulate most features of the human disease, and support a tumour-suppressor role of Men1.

Gene expression

Mammalian SWI/SNF complexes promote MyoD-mediated muscle differentiation. De la Serna, I. L. et al. Nature Genet . 27, 187–190 (2001) [PubMed]

The transcriptional regulator MyoD can induce fibroblasts to differentiate as muscle cells in culture. The process involves the activation of MyoD target genes, but what other molecules are required to switch on the right genes? These authors used an inducible dominant-negative version of a chromatin remodelling protein to show that the SWI/SNF chromatin remodelling complex is necessary for the induction of MyoD targets, and therefore for the initiation of a cellular differentiation programme.