Abstract

Organisms are locked in an eternal struggle with parasitic DNA sequences that live inside their genomes and wreak havoc on their host’s chromosomes as they spread through populations. To combat these parasites, host species have evolved elaborate mechanisms of resistance that suppress their activity. A new study in Drosophila indicates that, prior to the acquisition of resistance, individuals can vary in their ability to tolerate the activity of these genomic parasites, ignoring or repairing the damage they induce. This tolerance results from variation at genes involved in germline development and DNA damage checkpoints and suggests that these highly conserved cellular processes may be influenced by current and historical intragenomic parasite loads.

Highlights

  • In 1971, while crossing flies taken from natural populations with laboratory strains carrying visible markers, the Drosophila geneticist Yuichiro Hiraizumi observed unexpected recombination through males [8]

  • Kidwell and Sved made the crucial discovery that hybrid dysgenesis was controlled by an interaction between the maternal cytoplasm and elements residing on the paternal chromosomes

  • This was revealed by the fact that when males of strains established from natural populations (P strains) were mated with laboratory strain females (M strains), hybrid dysgenesis would occur, while the reciprocal cross of P strain females with laboratory M strain males did not induce dysgenesis

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Summary

OPEN ACCESS

Genetic maps identified precise coordinates for genes that followed the rules of mendelian segregation. Beginning in the 1940s, Barbara McClintock’s studies in maize revealed that the genome could be unruly [1,2]. Her groundbreaking work showed that autonomous and nonautonomous mobile elements could move throughout the genome, leaving behind them a trail of broken chromosomes and mutations. In the 1950s and ‘60s, studies using multiple species of Drosophila suggested that particular genotypes could have unstable genomes, with high rates of mutation and chromosomal breakage (for two excellent historical reviews, see [3,4]).

The mysterious P cytotype
Tolerant genomes
Findings
Beyond bruno
Full Text
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