The severe nuclear accident at Chernobyl in 1986 resulted in the worst reported accidental exposure of radioactive material to free-living organisms. Short-term effects on human populations inhabiting polluted areas include increased incidence of thyroid cancer, infant leukaemia, and congenital malformations in newborns. Two recent studies have reported, although with some controversy, that germline mutation rates were increased in humans and voles living close to Chernobyl, but little is known about the viability of the organisms affected. Here we report an increased frequency of partial albinism, a morphological aberration associated with a loss of fitness, among barn swallows, Hirundo rustica, breeding close to Chernobyl. Heritability estimates indicate that mutations causing albinism were at least partly of germline origin. Furthermore, evidence for an increased germline mutation rate was obtained from segregation analysis at two hypervariable microsatellite loci, indicating that mutation events in barn swallows from Chernobyl were two- to tenfold higher than in birds from control areas in Ukraine and Italy.

No abstract

In many vertebrates, males are apparently more affected by adverse environmental conditions, particularly during early stages of development, than are females. Three explanations have been proposed for this pattern. First, sexual size dimorphism (SSD) may result in sexes having different nutritional requirements to achieve the same viability, and males are more commonly the larger sex. Second, reduced performance of males could result from possession of an unguarded sex chromosome combined with environmental dependence in expression of deleterious recessives. Third, the obsesrved difference may be a consequence of possession of a male phenotype, for example, due to higher circulating levels of androgens associated with development of male reproductive organs acting antagonistically on other systems. We used experimental manipulations of rearing conditions, coupled with a molecular genetic technique for gender identification, to test these hypotheses in a population of Collared Flycatchers, Ficedula albicollis, a migrant, hole‐nesting passerine bird. Nestlings of that species exhibit sexual size monomorphism, and as with other birds, females are heterogametic. As a consequence, the three hypotheses make different predictions about the way in which gender and the environment will interact. Comparisons of brothers and sisters in a split‐brood, partial cross‐fostering design revealed no evidence of gender × environment interaction on body size, wing length, body mass, or recruitment to the breeding population in this size monomorphic species. Our results therefore support the first hypothesis, namely, that sex differences in performance in sexually dimorphic species are most likely to be caused by different nutritional requirements. Our experiments allow us to investigate the existence of sex‐specific fitness differences across an environmental gradient; such data are important for generating and testing hypotheses relating to adaptive sex allocation. The absence of gender × environment interactions demonstrated here supports recent studies of this species indicating a lack of sex ratio adjustment in response to a related, natural, environmental gradient. The possibility of gender × environment interactions along environmental gradients other than those investigated here should be addressed experimentally.

A primary male autosomal linkage map of the domestic horse (Equus caballus) has been developed by segregation analysis of 140 genetic markers within eight half-sib families. The family material comprised four Standardbred trotters and four Icelandic horses, with a total of 263 offspring. The marker set included 121 microsatellite markers, eight protein polymorphisms, five RFLPs, three blood group polymorphisms, two PCR–RFLPs, and one single strand conformation polymorphism (SSCP). One hundred markers were arranged into 25 linkage groups, 22 of which could be assigned physically to 18 different chromosomes (ECA1, ECA2, ECA3, ECA4, ECA5, ECA6, ECA7, ECA9, ECA10, ECA11, ECA13, ECA15, ECA16, ECA18, ECA19, ECA21, ECA22, and ECA30). The average distance between linked markers was 12.6 cM and the longest linkage group measured 103 cM. The total map distance contained within linkage groups was 679 cM. If the distances covered outside the ends of linkage groups and by unlinked markers were included, it was estimated that the marker set covered at least 1500 cM, that is, at least 50% of the genome. A comparison of the relationship between genetic and physical distances in anchored linkage groups gave ratios of 0.5–0.8 cM per Mb of DNA. This would suggest that the total male recombinational distance in the horse is 2000 cM; this value is lower than that suggested by chiasma counts. The present map should provide an important framework for future genome mapping in the horse.

Twenty equine microsatellites were isolated from a genomic phage library, and their genetical and physical localization was sought by linkage mapping and fluorescent in situ hybridization (FISH). Nineteen of the markers were found to be polymorphic with, in most cases, heterozygosities exceeding 50%. The markers were mapped in a Swedish reference family for gene mapping, comprising eight half-sib families from Standardbred and Icelandic horse sires. Segregation was analyzed against a set of 35 other markers typed in the pedigree. Thirteen of the microsatellites showed linkage to at least one other marker, with a total of 21 markers being involved in these linkages. In parallel, 18 of the microsatellites could be assigned to their chromosomal region by FISH. These assignments involved eight equine autosomes: ECA1, 2, 4, 6, 9, 10, 15, and 16. The genetical and physical mappings revealed by this study represent a significant extension of the current knowledge of the equine genome map.