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The Role of Parental Origin of Chromosomes in the Instability of the Somatic Genome in Drosophila Brain Cells and Memory Trace Formation in Norm and Stress
Cell and Tissue Biology Pub Date : 2020-06-03 , DOI: 10.1134/s1990519x20030074
S. A. Vasilieva , E. V. Tokmacheva , A. V. Medvedeva , A. A. Ermilova , E. A. Nikitina , B. F. Shchegolev , S. V. Surma , E. V. Savvateeva-Popova

Abstract—

It is impossible to imagine the nervous system without controllable genome instability, resulting in brain somatic mosaicism, one of the basic mechanisms of structural and functional heterogeneity of neurons. The source of such an instability is the presence of “hot spots” (repeating DNA sequences, provoking nonallelic recombination) and double-strand (DS) DNA breaks in the genome that occur in the matrix processes and physiological activity of neurons and are involved in memory formation and learning. The realization of the “norm–pathology” scenario is under epigenetic control; in particular, it depends on the parental effect of genome origin and stress. In this work, using the Williams model of drosophila carrying the agnts3 mutation in the gene for LIMK1 (the key enzyme of actin remodeling) using reciprocal hybrids with wild-type Canton-S line, we studied the contribution of maternal and paternal genomes in processes of learning and memory, as well as the formation of chromosome rearrangement in neuroblasts, determined by DS breaks and disorders of mitotic apparatus in norm and in exposure to stress impact via weak static magnetic field. The prevalent role of paternal genome in memory trace formation is shown. A patroclinous inheritance is established for frequencies of chromosome rearrangements and DS breaks, as well as chromatid bridges in anaphase neuroblasts at stress in the case of paternal agnts3 line. In the breed of agnts3 females, mitosis disorders are inherited via the maternal type. Based on previous research, we revealed microRNA contexts that can make patroclinous effects possible.


中文翻译:

染色体的父母起源在果蝇脑细胞中体细胞基因组的不稳定性以及正常和压力下的记忆痕迹形成中的作用

摘要-

无法想象没有可控制的基因组不稳定的神经系统会导致大脑体细胞镶嵌,这是神经元结构和功能异质性的基本机制之一。这种不稳定性的根源是基因组中出现“热点”(重复DNA序列,引起非等位基因重组)和基因组中双链(DS)DNA断裂,这些断裂发生在神经元的基质过程和生理活动中,并参与其中。记忆形成和学习。“规范病理学”情景的实现处于表观遗传控制之下;特别地,这取决于基因组起源和压力的父母效应。在这项工作中,利用果蝇携带威廉姆斯模型AGN TS3使用与野生型Canton-S系互易杂交的LIMK1(肌动蛋白重塑的关键酶)基因的突变,我们研究了母本和父本基因组在学习和记忆过程中的贡献以及染色体重排的形成在成神经细胞中,由DS断裂和有丝分裂器的失常所决定,这是正常情况下以及通过弱静磁场暴露于压力影响下的。显示了父本基因组在记忆痕迹形成中的普遍作用。甲patroclinous继承在应力在父系的情况下建立了在后期神经母细胞的染色体重排和DS断裂,以及染色单体桥的频率AGN TS3线。在品种AGN TS3女性,有丝分裂障碍是通过母体类型遗传的。根据先前的研究,我们揭示了可以使巡花效应成为可能的microRNA环境。
更新日期:2020-06-03
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