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The redusome hypothesis of aging and the control of biological time during individual development

机译:衰老的重做假设和个体发育过程中生物时间的控制

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The redusome hypothesis of aging and the control of biological time in individual development is proposed. Redusomes are hypothetical perichromosomal particles arising in differentiation events during morphogenesis of an organism The linear molecule of DNA covered with proteins in the redusome is assumed to be a copy of a segment of chromosomal chromosome even in the course of cellular divisions, being kept in its chromosomal nest. The redusome does not leave the body of a chromosome even in the course of cellular divisions, being kept in its chromosomal nest. Like telomeric DNA, redusome linear DNA is shortened step by step. Thus, tiny redusomes progressively decrease in size; it is from here their name originates. Together with loss of the length of DNA in a redusome, the number of different genes contained in it also decreases. Shortening of the redusomal DNA molecules (and, coupled to it, changes of the sets of genes in redusomes) is responsible for age-dependent shifts in the level of expression of different chromosomal genes. Owing to this, redusome DNA shortening serves as a key means of measuring biological time in individual development. The main part of DNA of most redusomes is postulated to be occupied by noncoding genes. Low-molecular-weight RNAs (micro RNAs and fountain RNAs, or fRNAs) are assumed to be transcribed from them. These RNAs are involved in regulation of various chromatin repacking that are specific to certain differentiations, while others modulate the levels of expression of chromosomal genes. Hypothetical fountain RNAs can quantitatively regulate the expression levels of chromosomal genes, forming specific complexes with fions. Fions are suggested to be specific sites of a chromosomal DNA which are complementary to different fRNAs. Fions reside in the vicinity of usual chromosomal genes. A complex of the fRNA-fion, specifically interacting with a closed gate of the corresponding ion channel of the internal nuclear mebrane, initiates the opening of the gate for a very short time, thus organizing activity of an ion fountain which appears to be automaticaly aimed at the chromosomal gene nearest to the fion involved. The ion fountain creates, depending on specificity of matching fRNA, fion, and ion channel, a distinctive ionic environment near certain structural genes. Ion fountains exert their action on the configuration of corresponding segments of chromatin and on the transcriptional efficiency of chromosomal genes in a topographically specific manner. Hence, the fountain system of the nucleus is able to regulate the quantitative traits both of cells and organism; it can control dominance of alleles and plays a role in individual development. Significant and escalating truncation of the redusome DNA causes cell aging due to an arising and increasing deficit of fRNAs and, for this reason, the lack of required ions near certain structural genes. Progressive shortening of DNA of redusomes is proposed to result in cellular aging because of a constantly growing shortage of low-molecular-weight RNAs transcribed from redusomal genes. Two types of redusomes are postulated: chronosomes and printosomes. Linear molecules of DNA in these two types of redusomes are called chronomeres and printomeres, respectively. Chronosomes are responsible for measurement of biological time in nondividing cells of the CNS. Printosomes remember positions of cells in the course of interpretation of the positional information in morphogenesis. In accordance with the position of a cell in a morphogenetic field, printomeres do change cellular properties and remember the change made (this is a so-called printomere mechanism of interpretation of positional information). Besides, printomeres participate in maintaining the achieved state of cellular differentiation. Normally, the chronomere is shortened only on the maximum of infradian hormonal rhythm (T-rhythm) which initiates the act of a superhigh velocity of its transcription that
机译:提出了衰老的重用假设和个体发育中生物时间的控制。重做组是在生物体形态发生过程中的分化事件中产生的假想染色体周围颗粒。重做组中被蛋白质覆盖的线性DNA分子即使在细胞分裂过程中也被认为是染色体染色体片段的副本,并保持其染色体状态巢。即使在细胞分裂的过程中,重做组也不会离开染色体,而是保留在其染色体巢中。像端粒DNA一样,重排线性DNA会逐步缩短。因此,微小的重做组逐渐减小了大小;他们的名字是从这里起源的。连同重做组中DNA长度的减少,其中包含的不同基因的数量也减少了。 Redusomal DNA分子的缩短(以及与其相关的Redusomes中基因组的变化)是导致不同染色体基因表达水平随年龄变化的原因。因此,缩短重复基因组DNA成为衡量个体发育中生物时间的关键手段。假定大多数重做组的DNA的主要部分被非编码基因占据。低分子量RNA(微小RNA和喷泉RNA,或fRNA)被认为是从它们转录而成的。这些RNA参与特定于某些分化的各种染色质重排的调控,而其他RNA则调节染色体基因的表达水平。假设的喷泉RNA可以定量调节染色体基因的表达水平,与假蝇形成特定的复合物。 Fions被认为是染色体DNA的特定位点,与不同的fRNA互补。幼犬生活在通常的染色体基因附近。 fRNA-fion的复合物,特别是与内部核膜相应离子通道的封闭门相互作用,会在很短的时间内启动该门的打开,从而组织似乎自动瞄准的离子源的活动位于最接近相关基因的染色体基因上。根据匹配的fRNA,fion和离子通道的特异性,离子源会在某些结构基因附近创建一个独特的离子环境。离子源以拓扑特定的方式对染色质相应片段的构型和染色体基因的转录效率发挥作用。因此,核的泉源系统能够调节细胞和生物体的数量特征。它可以控制等位基因的优势并在个体发育中发挥作用。由于fRNA的出现和增加的缺乏,并且由于某些原因,某些结构基因附近缺少必需的离子,导致重组DNA的显着且不断增加的截断会导致细胞衰老。由于从重定基因转录的低分子量RNA的持续短缺,提出了重定基因组DNA的逐步缩短以导致细胞衰老。假定有两种类型的Redusome:计时体和印刷体。这两种类型的Redusome中的线性DNA分子分别称为chronomeres和printomeres。染色体负责中枢神经系统非分裂细胞中生物时间的测量。体小体在解释形态发生中的位置信息的过程中记住细胞的位置。根据细胞在形态发生场中的位置,印刷异构体确实会改变细胞特性并记住所做的改变(这是解释位置信息的所谓印刷异构体机制)。此外,印刷异构体参与维持细胞分化的状态。通常情况下,仅在最大的下颌荷尔蒙节律(T-rhythm)时,才将发色团缩短。

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