Viability of X-autosome translocations in mammals: an epigenomic hypothesis from a rodent case-study
Viability of X-autosome translocations in mammals: an epigenomic hypothesis from a rodent case-study
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DOI：
10.1007/s00412-004-0292-6
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发表时间：
2004-08-01
期刊：
影响因子：
1.6
通讯作者：
Volobouev, V
中科院分区：
文献类型：
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作者：
Dobigny, G;Ozouf-Costaz, C;Volobouev, V
X-常染色体易位是由于减数分裂破坏、X-失活对常染色体的影响以及在两个区段之间维持不同复制定时模式的必要性而引起的高度有害的染色体重排。尽管如此，X-常染色体易位并不罕见。我们在这里集中在属Taterillus（啮齿目，沙鼠），提供了两个姐妹谱系不同的两个常染色体-生殖体易位。尽管最近和戏剧性的染色体重新图案化这些谱系的特点，X-常染色体易位的物种都显示常染色体和祖先的性节段之间的插入异染色质块（IHB）。这些区块，由高度扩增的端粒重复序列和rDNA簇组成，在非易位物种的染色体上没有观察到，易位物种的Y1和Y2也没有观察到。这种IHB存在于所有记录X-常染色体易位的哺乳动物中。我们提出了一个表观基因组假说，解释了哺乳动物中X-常染色体易位的可行性。这表明，组成型异染色质可能是X染色体常染色体易位的选择，因为它可以（1）防止失活X染色体的兼性异染色质化扩散到常染色体部分，（2）允许独立调节性和常染色体片段的复制时间。
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.