Condensin recruitment to chromatin is inhibited by Chk2 kinase in response to DNA damage.

The DNA damage checkpoint, when activated in response to genotoxic damage during S phase, arrests cells in G2 phase of the cell cycle. ATM, ATR, Chk1 and Chk2 kinases are the main effectors of this checkpoint pathway. The checkpoint kinases prevent the onset of mitosis by eliciting well characterized inhibitory phosphorylation of Cdk1.

A novel cell cycle inhibitor stalls replication forks and activates S phase checkpoint.

DNA replication checkpoint is activated in response to replication stresses. It maintains the integrity of stalled replication forks and prevents premature segregation of largely unreplicated chromosomes. In budding yeast, Mec1 and Rad53 kinases (homologous to mammalian ATM/ATR and Chk2 kinases, respectively) are the main effectors of this checkpoint control.

Molecular distinction between pathogenic and infectious properties of the prion protein.

Tg(PG14) mice express a prion protein (PrP) with a nine-octapeptide insertion associated with a human familial prion disease. These animals spontaneously develop a fatal neurodegenerative disorder characterized by ataxia, neuronal apoptosis, and accumulation in the brain of an aggregated and weakly protease-resistant form of mutant PrP (designated PG14(spon)). Brain homogenates from Tg(PG14) mice fail to transmit disease after intracerebral inoculation into recipient mice, indicating that PG14(spon), although pathogenic, is distinct from PrP(Sc), the infectious form of PrP.

Kinetic analysis of the interaction between the QutA and QutR transcription-regulating proteins.

The QutR protein is a multidomain repressor protein that interacts with the QutA activator protein. Both proteins are active in the signal transduction pathway that regulates transcription of the quinic acid utilization (qut) gene cluster of the microbial eukaryote Aspergillus nidulans. In the presence of quinate, production of mRNA from the eight genes of the qut pathway is stimulated by the QutA activator protein.

Production of transgenic rodents by the microinjection of cloned DNA into fertilized one-cell eggs.

Transgenic technologies that enable rapid movement between genotype and phenotype through specific loss-of-function, overexpression, or misexpression phenotypes will be crucial in the elucidation of gene sequences emerging from genome projects. This article describes detailed procedures for the generation of transgenic mice and rats by the injection of cloned DNA into the pronuclei of fertilized one-cell eggs.