缓行
蛋白质组
转录组
隐生
生物
DNA修复
计算生物学
DNA损伤
PARP1
烟酰胺腺嘌呤二核苷酸
基因
NAD+激酶
细胞生物学
DNA
聚ADP核糖聚合酶
生物化学
聚合酶
遗传学
酶
基因表达
植物
干燥
作者
Lei Li,Z. W. Ge,Shihao Liu,Kun Zheng,Yaqi Li,Kaiqi Chen,Yesheng Fu,Xiaoguang Lei,Zeling Cui,Yifan Wang,Jin Huang,Yanyan Liu,Mu Duan,Zimei Sun,Jun Chen,Liangwei Li,Pan Shen,Guibin Wang,Junmiao Chen,Ruochong Li
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2024-10-24
卷期号:386 (6720): eadl0799-eadl0799
被引量:45
标识
DOI:10.1126/science.adl0799
摘要
Tardigrades are captivating organisms known for their resilience in extreme environments, including ultra-high-dose radiation, but the underlying mechanisms of this resilience remain largely unknown. Using genome, transcriptome, and proteome analysis of Hypsibius henanensis sp. nov. , we explored the molecular basis contributing to radiotolerance in this organism. A putatively horizontally transferred gene, DOPA dioxygenase 1 ( DODA1 ), responds to radiation and confers radiotolerance by synthesizing betalains—a type of plant pigment with free radical–scavenging properties. A tardigrade-specific radiation-induced disordered protein, TRID1, facilitates DNA damage repair through a mechanism involving phase separation. Two mitochondrial respiratory chain complex assembly proteins, BCS1 and NDUFB8, accumulate to accelerate nicotinamide adenine dinucleotide (NAD + ) regeneration for poly(adenosine diphosphate–ribosyl)ation (PARylation) and subsequent poly(adenosine diphosphate–ribose) polymerase 1 (PARP1)–mediated DNA damage repair. These three observations expand our understanding of mechanisms of tardigrade radiotolerance.
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