Wang Jie, Zhang Guangpu, Sun Cheng, Chang Liming, Wang Yingyong, Yang Xin, Chen Guiying, Itgen Michael W, Haley Ava, Tang Jiaxing, Mueller Rachel Lockridge
Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu, Sichuan, China.
College of Life Sciences, Capital Normal University, Beijing, China.
Commun Biol. 2025 May 6;8(1):704. doi: 10.1038/s42003-025-08127-3.
Size evolution among gigantic genomes involves gain and loss of many gigabases of transposable elements (TEs), sequences that parasitize host genomes. Vertebrates suppress TEs using piRNA and KRAB-ZFP pathways. TEs and hosts coevolve in an arms race, where suppression strength reflects TE fitness costs. In enormous genomes, additional TE costs become miniscule. How, then, do TEs and host suppression invoke further addition of massive DNA amounts? We analyze TE proliferation histories, deletion rates, and community diversities in six salamander genomes (21.3 - 49.9 Gb), alongside gonadal expression of TEs and suppression pathways. We show that TE activity is higher in testes than ovaries, attributable to lower KRAB-ZFP suppression. Unexpectedly, genome size and expansion are uncorrelated with TE deletion rate, proliferation history, expression, and host suppression. Also, TE community diversity increases with genome size, contrasting theoretical predictions. We infer that TE-host antagonism in gigantic genomes produces stochastic TE accumulation, reflecting noisy intermolecular interactions in huge genomes and cells.
巨大基因组之间的大小演化涉及许多千兆碱基的转座元件（TEs）的得失，转座元件是寄生于宿主基因组的序列。脊椎动物利用piRNA和KRAB-ZFP途径抑制转座元件。转座元件和宿主在一场军备竞赛中共同进化，其中抑制强度反映了转座元件的适应性成本。在巨大的基因组中，额外的转座元件成本变得微不足道。那么，转座元件和宿主抑制是如何导致大量DNA进一步增加的呢？我们分析了六个蝾螈基因组（21.3 - 49.9Gb）中转座元件的增殖历史、缺失率和群落多样性，以及转座元件和抑制途径的性腺表达。我们发现，睾丸中转座元件的活性高于卵巢，这是由于KRAB-ZFP抑制作用较低。出乎意料的是，基因组大小和扩张与转座元件的缺失率、增殖历史、表达以及宿主抑制无关。此外，转座元件群落多样性随基因组大小增加，这与理论预测相反。我们推断，巨大基因组中转座元件与宿主的拮抗作用会导致随机的转座元件积累，这反映了巨大基因组和细胞中分子间相互作用的噪声。
