Evolutionary relationships across taxa can be deduced from sequence divergence of proteins, RNA, or DNA; sequences which diverge rapidly, such as those of mitochondrial genes, have been especially useful for comparisons of closely related species, and--within limits--of strains within a species. We have utilized the transposable element Tc1 as a polymorphic marker to evaluate the evolutionary relationships among nine Caenorhabditis elegans strains. For five low-Tc1-copy strains, we compared patterns of restriction fragments hybridizing to a cloned Tc1 probe. Twenty of the 40 Tc1 insertion sites thus characterized were common to all five strains, and so presumably preceded strain divergence; the 20 differential bands were used to construct a maximum-parsimony tree relating these strains. In four high-copy-number stocks (three wild-type strains and a subline), we determined occupancy of 35 individual Tc1 insertion sites by a polymerase chain reaction assay. Surprisingly, the high-copy strains share a common subset of these Tc1 insertions, and the chromosomal distribution of conserved Tc1 sites is "clustered" with respect to the other elements tested. These data imply a close evolutionary relationship among the high-copy strains, such that two of these strains appear to have been derived from the highest-copy-number lineage (represented by two stocks) through crossing with a low-Tc1 strain. Abundances of Tc1 elements were also estimated for the four high-copy-number stocks, at approximately 200-500 copies per haploid genome, by quantitative dot-blot hybridization relative to two low-copy strains. Annealing with 32P-labeled probes corresponding to full-length Tc1, an oligonucleotide within the Tc1 terminal inverted repeats, and an internal Tc1 oligonucleotide, gave essentially identical results--indicating that Tc1 termini exist in the genome primarily as components of full-length Tc1 elements. A composite evolutionary tree is proposed, based on the locations and numbers of Tc1 elements in these strains, which is consistent with a four-branch intraspecific tree deduced previously by maximum-parsimony analyses of mitochondrial sequence changes; it also serves to elucidate the evolutionary history of transposon mobility.

The potential for recovery from the cortical effects of monocular deprivation (MD) was studied in kittens that were briefly deprived and then exposed to various periods of normal binocular vision. In eight kittens, recordings from the hemisphere ipsilateral to the deprived eye revealed that at 4 wk of age, exposure to 12 h of MD (six 2-h sessions spread over 2 days) was sufficient to cause a massive shift in the ocular dominance of striate cortex neurons in favor of the nondeprived eye. Six of these MD kittens were allowed 3 wk of normal binocular vision and then recorded from a second time to assess the extent to which their cortex could recover from the effects of this brief period of deprivation. Data from these animals indicated that now approximately equal numbers of cortical neurons were dominated by each eye and that, while the overall level of binocularity was somewhat lower than that found in normally reared animals, the majority of cells had regained functional binocular connections. The possibility that cortical binocularity could recover even further was explored by allowing four of these six MD kittens to experience an additional 4 wk of binocular vision and then recording from them a third time. These final recordings indicated that following a total of 7 wk of binocular vision, the level of cortical binocularity was no different from that found in normally reared animals. Having demonstrated that normal binocular function can be restored to a cortex in which it had been severely disrupted, we next attempted to characterize the earliest stages of this recovery process by examining the pattern of cortical binocularity in 10 MD kittens that were allowed to experience either 6 or 12 h of binocular vision (given over 1 or 2 days, respectively). Our results indicate that, during the initial day of binocular vision, recovery seems to involve a noncompetitive expansion of functional cortical input from the deprived eye, which joins with input from the nondeprived eye in driving cortical neurons. The level of cortical binocularity continues to increase during the next day of binocular vision, but now there is also a small increase in the proportion of cells driven exclusively by the initially deprived eye--suggesting that there may be an additional competitive component to the early stages of recovery. The results of this study complement our previous report of complete recovery of binocularity following exposure to a brief period of optically induced strabismus.(ABSTRACT TRUNCATED AT 400 WORDS)

We previously identified five regions on the chromosomal map of Caenorhabditis elegans, containing genes that help specify life span in this species, by comparing the genotypes of young and long‐lived progeny from a cross between strains Bristol‐N2 and Bergerac‐BO [Ebert et al. (1993): Genetics 135:1003–1010]. Analyses of additional crosses, and of putative polymorphisms for the implicated genes, are necessary to clarify the roles of naturally occurring polymorphic alleles in determining longevity. We therefore carried out a second multigenerational cross, between strains Bristol‐N2 and DH424 (both nonmutators at 20°C), to create a different heterogeneous recombinant‐inbred population. We again found strong evidence implicating multiple genes, which differ between the parental strains, in the determination of life span. Increased variance of survival, for F2 and homozygous F25 worms relative to F1 hybrids, is consistent with such alleles assorting randomly in the cross progeny. Moreover, chromosome mapping data corroborate the polygenic nature of this quantitative trait. Genotypes of young and very long‐lived adult worms from a synchronous F15 population were determined by polymerase chain reaction, to identify the parental strain of origin for each of 10 polymorphic loci. Two regions, on chromosomes II and IV, each contain at least one gene with allelic differences in associated longevity. A recombinant‐inbred Bergerac‐BO × Bristol‐N2 population, derived from the earlier cross between those strains, was exposed to an acute toxic level of hydrogen peroxide. Genotyping of H2O2‐resistant worms implicated at least one of the five chromosomal regions previously identified in the same cross progeny as harboring a longevity‐determining gene. Superoxide dismutase and catalase levels, determined for the three parental strains as they aged, confirm the existence of polymorphisms in the corresponding genes (or their regulatory mechanisms) inferred from the chromosome‐II mapping data, and are consistent with the hypothesis that increased longevity is conferred by high levels of these enzymes late in life. © 1996 Wiley‐Liss, Inc.