Development

Xenopus Sprouty2 inhibits FGF-mediated gastrulation movements but does not affect mesoderm induction and patterning. Nutt, S. L. et al. Genes Dev. 15 , 1152–1166 (2001) [PubMed]

Fibroblast growth factor (FGF)-mediated signalling is required for specifying the vertebrate body plan. Sprouty acts as an antagonist of FGF signalling. But whereas Drosophila melanogaster Sprouty inhibits the Ras/mitogen-activated protein kinase (MAPK) pathway, the newly cloned Xenopus laevis sprouty2 gene product, Xspry2, inhibits calcium mobilization. This paper provides evidence for the existence of at least two FGF-dependent pathways involved in Xenopus mesoderm patterning and morphogenesis.

Cancer

A novel role for the Bcl-2 protein family: specific suppression of the RAD51 recombination pathway. Saintigny, Y. et al. EMBO J. 20 , 2596–2607 (2001) [PubMed]

Bcl-2, famous for its anti-apoptotic activity, now has a new role as a genetic mutator. It does this by inhibiting the Rad51-dependent conservative recombination pathway, probably by affecting post-translational modification of the Rad51 protein. As this occurs independently of the ability of Bcl-2 to repress apoptosis through its association with Bax, these new results now indicate that Bcl-2 can confer a cancer-prone phenotype by two separate means.

Oxidative stress

Role of ATM in oxidative stress-mediated c-Jun phosphorylation in response to ionizing radiation and CdCl2. Lee, S. A. et al. J. Biol. Chem. 276 , 11783–11790 (2001) [PubMed]

The ataxia telangiectasia gene product is required for oxidative stress-induced G1 and G2 checkpoint function in human fibroblasts. Shackelford, R. E. et al. J. Biol Chem. 17 April (2001) (epub ahead of print)

Elevated Cu/Zn-SOD exacerbates radiation sensitivity and hematopoietic abnormalitities of Atm-deficient mice. Peter, Y. et al. EMBO J. 20 , 1538–1546 (2001) [PubMed]

Some of the phenotypes observed in ataxia telangiectasia (AT) patients — sensitivity to ionizing radiation and cancer predisposition — are thought to result from a failure of cells to respond to oxidative damage. Three groups now provide a molecular basis for this, showing that the gene mutated in AT, ATM, responds to oxidative damage by triggering G1 and G2 cell-cycle checkpoints, the induction of p53 and the activation of c-Jun by phosphorylation. Accordingly, elevated levels of Cu/Zn superoxide dismutase exacerbate radiation sensitivity in ATM-deficient mice.