What is a schizophrenic mouse?

In this issue of Neuron, Clapcote et al. examine mice containing missense mutations of the DISC1 gene, a locus associated with major mental illness in at least one large Scottish family. Genetic manipulation of mouse homologs of genes implicated in the etiology of psychiatric disorders is a promising avenue of research, but also one that is fraught with interpretative difficulties.     

A bigger mouse? The rat genome unveiled

Rattus norvegicus is an important experimental organism and interesting to evolutionary biologists. The recently published draft rat genome sequence provides us with insights into both the rat's evolution and its physiology. We learn more about genome evolution and, in particular, the adaptive significance of gene family expansions and the evolution of rodent genomes, which appears to have decelerated since the divergence of mouse and rat. An important observation is that some regions of genomes, many in noncoding regions, show very high sequence conservation, while others show unexpectedly fast evolution. Both of these may be pointers to functional significance.     

Are mouse telomeres going to pot?

Pot1 is a conserved single-stranded DNA binding protein with crucial functions in the protection of telomeres and maintenance of their length. In this issue of Cell, two papers (Hockemeyer et al., 2006; Wu et al., 2006) examine the roles of murine Pot1 homologs and describe intriguing new insights into how cells protect their chromosome ends from DNA-repair activities.     

Honest signaling in mouse lemur vocalizations?

International Journal of Primatology - Animal vocalizations may provide information about a sender’s condition or motivational state and, hence, mediate social interactions. In this study, we...     

Does my mouse have Alzheimer's disease?

Small animal models that manifest many of the characteristic neuropathological and behavioral features of Alzheimer's disease (AD) have been developed and have proven of great value for studying the pathogenesis of this disorder at the molecular, cellular and behavioral levels. The great progress made in our understanding of the genetic factors that either cause or contribute to the risk of developing AD has prompted many laboratories to create transgenic (tg) mice that overexpress specific genes which cause familial forms of the disease. Several of these tg mice display neuropathological and behavioral features of AD including amyloid β-peptide (Aβ) and amyloid deposits, neuritic plaques, gliosis, synaptic alterations and signs of neurodegeneration as well as memory impairment. Despite these similarities, important differences in neuropathology and behavior between these tg mouse models and AD have also been observed, and to date no perfect animal model has emerged. Moreover, ascertaining which elements of the neuropathological and behavioral phenotype of these various strains of tg mice are relevant to that observed in AD continues to be a challenge. Here we provide a critical review of the AD-like neuropathology and behavioral phenotypes of several well-known and utilized tg mice that express human APP transgenes.     

Is mouse embryonic stem cell technology obsolete?

Injection of recombinant Cas9 protein and synthetic guide RNAs into mouse zygotes has been shown to facilitate gene disruption and knock-ins using the CRISPR system. These technologies may soon displace genetic modification using embryonic stem cells.     

Computational genetics: from mouse to human?

In this article, we describe a novel computational-analysis method that rapidly identified the genetic basis for several trait differences among inbred mouse strains. This approach enables researchers to identify a causative genetic factor by correlating a pattern of observable physiological or pathological differences among selected inbred strains with a pattern of genetic variation. Compared with conventional methods used for mouse genetic analysis, which require many years to produce results, this haplotype-based computational analysis can be rapidly performed. We discuss the factors affecting the performance and precision of this computational method. Although it currently can analyze traits of limited genetic complexity in mouse, the potential application of this genetic-analysis method to other experimental organisms, and possibly humans, is evaluated.     

When did the house mouse colonize Europe?

This paper is a reply to a recent proposal by Sage and co-workers giving an early date for the colonization of Europe by the house mouse, based on mitochondria! DNA nucleotide divergence estimates. The large discrepancy in time between the date given by these authors and our own is discussed in the light of available palaeontological and genetic data. This leads us to reject the hypothesis supported by Sage and co-workers, and suggest a much more recent date of colonization.     

Is the genotype-phenotype map modular? A statistical approach using mouse quantitative trait loci data.

Various theories about the evolution of complex characters make predictions about the statistical distribution of genetic effects on phenotypic characters, also called the genotype-phenotype map. With the advent of QTL technology, data about these distributions are becoming available. In this article, we propose simple tests for the prediction that functionally integrated characters have a modular genotype-phenotype map. The test is applied to QTL data on the mouse mandible. The results provide statistical support for the notion that the ascending ramus region of the mandible is modularized. A data set comprising the effects of QTL on a more extensive portion of the phenotype is required to determine if the alveolar region of the mandible is also modularized.