In this paper we review and integrate key aspects of behavioral and life history traits, food supply and population dynamics of the white-footed mouse (Peromyscus leucopus), a species that is abundant and widely distributed across much of eastern North America. Results are based largely on a 33-year mark-and-recapture study in a forest fragment in northwest Ohio, USA. Behavioral plasticity in such reproductive traits as mating system and parental care allows this species to adjust quickly to changing environments. The species has a relatively "fast" life history, with rapid attainment of sexual maturity and high fecundity in the face of high mortality rates. Maximal reproductive effort early in life enables a rapid population response. Food supply, in the form of mast, determines the size of the reproducing population in early spring, which, in turn, influences the size of the late summer peak population. The peak population size is also affected by short-term weather events possibly acting via the food supply. The effects of weather and food on population growth are in part mediated through competition, including defense of space and suppression of reproduction. The inelasticity of female territories appears to set an upper limit to population density.

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Two genomic clones exhibiting a maternal-specific pattern of expression map to cytological region 52A. To elucidate the function of these clones we have undertaken a mutagenesis of the cytological region 51D-52A. This paper presents the results of this screen and the preliminary analysis of female-sterile and lethal mutations isolated. A total of twelve complementation groups have been identified, four of which are defined exclusively by female-sterile alleles. Only one visible mutation was isolated, a recessive temperature-sensitive allele of Thickened-arista (Tarts). Several of the seven lethal loci display an embryonic lethal phase. Three of the four female-sterile loci affect chorion structure with one resulting in underamplification of the chorion genes, and two (possibly three) of the four female-steriles affect nuclear division/DNA replication. Thus it appears that this is a "developmentally important" region, possibly representing a clustering of genes involved in either DNA replication or nuclear division.

Mutations in the maternal-effect gene abnormal chromatin (abc) in Drosophila melanogaster result in a variety of defects involving nuclear replication/division. Three recessive alleles of this gene, which maps near 51F on chromosome 2, all result in female sterility. They cause slower embryonic development that is usually abnormal from the earliest nuclear divisions and arrested by the sixth one. Nuclei tend to be large and erratically distributed, some intensely staining. Mitotic asynchrony is common. Few embryos reach the gastrula stage and none hatch. With the weakest allele, fsPL, bridges between nuclei are common; abnormal chromatin clumps that resemble yolk nuclei occur before the other nuclei reach the surface; and spindle anomalies and DNA wads with numerous centrosomes are seen. Females with the stronger alleles, fsA5 and fs27, lay fewer eggs and a smaller proportion of embryos reach blastoderm; developmental arrest occurs earlier, usually with several large nuclei distributed along the length of the embryo. Chorion defects occur in all three mutants. Mitotic asynchrony, nuclear bridging, endoreduplication and nuclear behavior aberrant from the first division suggest that the abc gene product operates in DNA replication/nuclear division. Larval (homozygous F1) neuroblast chromosome structure and mitotic indices are normal, indicating that any mitotic function is strictly maternal, i.e. abc is not a general mitotic gene. Thus abc is one of a few known genes with a maternal effect that appears to function in the embryonic cell cycle.