Abstract
Telomeres, specialised structures that protect chromosome ends, play a critical role in preserving chromosome integrity. Telomere dynamics in the Tasmanian devil (Sarcophilus harrisii) are of particular interest in light of the emergence of devil facial tumour disease (DFTD), a transmissible malignancy that causes rapid mortality and threatens the species with extinction. We used fluorescent in situ hybridisation to investigate telomere length in DFTD cells, in healthy Tasmanian devils and in four closely related marsupial species. Here we report that animals in the Order Dasyuromorphia have chromosomes characterised by striking telomere length dimorphism between homologues. Findings in sex chromosomes suggest that telomere length dimorphism may be regulated by events in the parental germlines. Long telomeres on the Y chromosome imply that telomere lengthening occurs during spermatogenesis, whereas telomere diminution occurs during oogenesis. Although found in several somatic cell tissue types, telomere length dimorphism was not found in DFTD cancer cells, which are characterised by uniformly short telomeres. This is, to our knowledge, the first report of naturally occurring telomere length dimorphism in any species and suggests a novel strategy of telomere length control. Comparative studies in five distantly related marsupials and a monotreme indicate that telomere dimorphism evolved at least 50 million years ago.
Highlights
Eukaryotic chromosome ends are capped by telomeres, specialised nucleoprotein structures that maintain chromosome stability, limit replicative lifespan, and in doing so, impact carcinogenesis and age-related degenerative disease [1,2,3,4]
We found that chromosomes from healthy Tasmanian devils are distinguished by striking differences in telomere length between homologous chromosomes
This is the first report of naturally occurring telomere length dimorphism in any species and reflects a novel strategy of telomere length control
Summary
Eukaryotic chromosome ends are capped by telomeres, specialised nucleoprotein structures that maintain chromosome stability, limit replicative lifespan, and in doing so, impact carcinogenesis and age-related degenerative disease [1,2,3,4]. Mice and yeast, current models propose that telomerase is limiting, and is preferentially targeted to the shortest telomeres [9,10,11]. Telomerase-positive cancer cell lines typically display short, homogeneous telomere lengths [12]. ALT-positive cancer cells are typified by strikingly heterogeneous telomeres and the presence of ALT-associated promyelocytic leukemia protein nuclear bodies (APBs) [13]. Some human neoplasms have both telomerase activity and chromosomes characterised by telomere length heterogeneity suggestive of ALT [14]
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