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Genome Biol Evol. 2014 May 19;6(6):1279-86. doi: 10.1093/gbe/evu104.

Recurrent turnover of chromosome-specific satellites in Drosophila.

Author information

1
Center for Integrative Bioinformatics Vienna (CIBIV), Max F. Perutz Laboratories, University of Vienna and Medical University of Vienna, Austria miguel.gallach@univie.ac.at.

Abstract

Repetitive DNA are DNA sequences that are repeated multiple times in the genome and normally considered nonfunctional. Several studies predict that the rapid evolution of chromosome-specific satellites led to hybrid incompatibilities and speciation. Interestingly, in Drosophila, the X and dot chromosomes share a unique and noteworthy property: They are identified by chromosome-specific binding proteins and they are particularly involved in genetic incompatibilities between closely related species. Here, I show that the X and dot chromosomes are overpopulated by certain repetitive elements that undergo recurrent turnover in Drosophila species. The portion of the X and dot chromosomes covered by such satellites is up to 52 times and 44 times higher than in other chromosomes, respectively. In addition, the newly evolved X chromosome in D. pseudoobscura (the chromosomal arm XR) has been invaded by the same satellite that colonized the ancestral X chromosome (chromosomal arm XL), whereas the autosomal homologs in other species remain mostly devoid of satellites. Contrarily, the Müller element F in D. ananassae, homolog to the dot chromosome in D. melanogaster, has no overrepresented DNA sequences compared with any other chromosome. The biology and evolutionary patterns of the characterized satellites suggest that they provide both chromosomes with some kind of structural identity and are exposed to natural selection. The rapid satellite turnover fits some speciation models and may explain why these two chromosomes are typically involved in hybrid incompatibilities.

KEYWORDS:

X chromosome; dosage compensation; dot chromosome; speciation

PMID:
24846631
PMCID:
PMC4079201
DOI:
10.1093/gbe/evu104
[Indexed for MEDLINE]
Free PMC Article

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