Research Article

Chromosoma

, Volume 113, Issue 1, pp 34-41

First online:

Viability of X-autosome translocations in mammals: an epigenomic hypothesis from a rodent case-study

  • G. DobignyAffiliated withLaboratoire Origine, Structure et Evolution de la Biodiversité, Muséum National d’Histoire NaturelleService de Systématique Moléculaire, MNHNEvolutionary Genomics Group, Department of Zoology, University of Stellenbosch Email author 
  • , C. Ozouf-CostazAffiliated withService de Systématique Moléculaire, MNHN
  • , C. BonilloAffiliated withService de Systématique Moléculaire, MNHN
  • , V. VolobouevAffiliated withLaboratoire Origine, Structure et Evolution de la Biodiversité, Muséum National d’Histoire Naturelle

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

Abstract

X-autosome translocations are highly deleterious chromosomal rearrangements due to meiotic disruption, the effects of X-inactivation on the autosome, and the necessity of maintaining different replication timing patterns between the two segments. In spite of this, X-autosome translocations are not uncommon. We here focus on the genus Taterillus (Rodentia, Gerbillinae) which provides two sister lineages differing by two autosome–gonosome translocations. Despite the recent and dramatic chromosomal repatterning characterising these lineages, the X-autosome translocated species all display intercalary heterochromatic blocks (IHBs) between the autosomal and the ancestral sexual segments. These blocks, composed of highly amplified telomeric repeats and rDNA clusters, are not observed on the chromosomes of the non-translocated species, nor the Y1 and Y2 of the translocated species. Such IHBs are found in all mammals documented for X-autosome translocation. We propose an epigenomic hypothesis which explains the viability of X-autosome translocations in mammals. This posits that constitutive heterochromatin is probably selected for in X-autosome translocations since it may (1) prevent facultative heterochromatinization of the inactivated X from spreading to the autosomal part, and (2) allow for the independent regulation of replication timing of the sex and autosomal segments.