Pilfering of stored seeds and the relative costs of scatter-hoarding versus larder-hoarding in yellow pine chipmunks

Yellow pine chipmunks ( Tamias amoenus ) scatter-hoard food during summer and autumn but must form a larder as a winter food source before winter begins. Yellow pine chipmunks do not larder-hoard large quantities of food during the summer, apparently because a summer larder could not be defended from pilferers. We tested the assumption that the rate of pilferage from an unguarded larder would be significantly greater than the rate of pilferage from surface caches (which are also unguarded by yellow pine chipmunks) during the summer and autumn. Buried plastic buckets were used as artificial nests containing larders of 1000 sunflower seeds or 200 Jeffrey pine ( Pinus jeffreyi ) seeds. The pilferage of larder contents was monitored daily and compared to pilferage of surface caches. Animals (yellow pine chipmunks and deer mice, Peromyscus maniculatus ) removed sunflower seeds from caches much faster than from larders, but caches of Jeffrey pine seeds disappeared much more slowly than pine seeds in larders. Further, animals removed pine seeds from larders more quickly than they did sunflower seeds from larders. The difference between seed species was probably because sunflower seeds have much stronger odors, which rodents readily detect, and because chipmunks prefer pine seeds over sunflower seeds. Yellow pine chipmunks must spend a considerable portion of their time foraging for seeds and may not be able to defend a large larder during summer.     

The genetic basis of family conflict resolution in mice

Asymmetries in the costs and benefits of parental investment for mothers, fathers and offspring result in family conflict over the production and provisioning of young. In species where females provide most resources before and after birth, the resolution of this conflict may be influenced by genes expressed in mothers and by maternally and paternally inherited genes expressed in offspring. Here we disentangle these effects by means of reciprocal mating and cross-fostering of litters between two strains of mice that differ with respect to the typical resolution of family conflict. We find that differences in litter size between these two strains are determined by paternal genotype, whereas differences in provisioning are under maternal control, showing that there is antagonistic coadaptation of maternal and paternal effects on distinct life-history traits. Maternal provisioning is also influenced by the type of foster offspring. Contradictory to theoretical expectations, however, we find no evidence for a negative correlation across strains between maternal provisioning and offspring demand. Instead, we show that there is positive coadaptation such that offspring obtain more resources from foster mothers of the same strain as their natural mother, irrespective of their father's strain.     

DNA damage defines sites of recurrent chromosomal translocations in B lymphocytes

Recurrent chromosomal translocations underlie both haematopoietic and solid tumours. Their origin has been ascribed to selection of random rearrangements, targeted DNA damage, or frequent nuclear interactions between translocation partners; however, the relative contribution of each of these elements has not been measured directly or on a large scale. Here we examine the role of nuclear architecture and frequency of DNA damage in the genesis of chromosomal translocations by measuring these parameters simultaneously in cultured mouse B lymphocytes. In the absence of recurrent DNA damage, translocations between Igh or Myc and all other genes are directly related to their contact frequency. Conversely, translocations associated with recurrent site-directed DNA damage are proportional to the rate of DNA break formation, as measured by replication protein A accumulation at the site of damage. Thus, non-targeted rearrangements reflect nuclear organization whereas DNA break formation governs the location and frequency of recurrent translocations, including those driving B-cell malignancies.     

Large-scale analysis of the yeast genome by transposon tagging and gene disruption

Economical methods by which gene function may be analysed on a genomic scale are relatively scarce. To fill this need, we have developed a transposon-tagging strategy for the genome-wide analysis of disruption phenotypes, gene expression and protein localization, and have applied this method to the large-scale analysis of gene function in the budding yeast Saccharomyces cerevisiae. Here we present the largest collection of defined yeast mutants ever generated within a single genetic background--a collection of over 11,000 strains, each carrying a transposon inserted within a region of the genome expressed during vegetative growth and/or sporulation. These insertions affect nearly 2,000 annotated genes, representing about one-third of the 6,200 predicted genes in the yeast genome. We have used this collection to determine disruption phenotypes for nearly 8,000 strains using 20 different growth conditions; the resulting data sets were clustered to identify groups of functionally related genes. We have also identified over 300 previously non-annotated open reading frames and analysed by indirect immunofluorescence over 1,300 transposon-tagged proteins. In total, our study encompasses over 260,000 data points, constituting the largest functional analysis of the yeast genome ever undertaken.