共查询到20条相似文献，搜索用时 281 毫秒
1.
Al Rawi S Louvet-Vallée S Djeddi A Sachse M Culetto E Hajjar C Boyd L Legouis R Galy V 《Science (New York, N.Y.)》2011,334(6059):1144-1147
In sexual reproduction of most animals, the spermatozoon provides DNA and centrioles, together with some cytoplasm and organelles, to the oocyte that is being fertilized. Paternal mitochondria and their genomes are generally eliminated in the embryo by an unknown degradation mechanism. We show that, upon fertilization, a Caenorhabditis elegans spermatozoon triggers the recruitment of autophagosomes within minutes and subsequent paternal mitochondria degradation. Whereas the nematode-specific sperm membranous organelles are ubiquitinated before autophagosome formation, the mitochondria are not. The degradation of both paternal structures and mitochondrial DNA requires an LC3-dependent autophagy. Analysis of fertilized mouse embryos shows the localization of autophagy markers, which suggests that this autophagy event is evolutionarily conserved to prevent both the transmission of paternal mitochondrial DNA to the offspring and the establishment of heteroplasmy. 相似文献
2.
Tsukamoto S Kuma A Murakami M Kishi C Yamamoto A Mizushima N 《Science (New York, N.Y.)》2008,321(5885):117-120
After fertilization, maternal proteins in oocytes are degraded and new proteins encoded by the zygotic genome are synthesized. We found that autophagy, a process for the degradation of cytoplasmic constituents in the lysosome, plays a critical role during this period. Autophagy was triggered by fertilization and up-regulated in early mouse embryos. Autophagy-defective oocytes derived from oocyte-specific Atg5 (autophagy-related 5) knockout mice failed to develop beyond the four- and eight-cell stages if they were fertilized by Atg5-null sperm, but could develop if they were fertilized by wild-type sperm. Protein synthesis rates were reduced in the autophagy-null embryos. Thus, autophagic degradation within early embryos is essential for preimplantation development in mammals. 相似文献
3.
应用DAPI、DiOC荧光法与激光共聚焦电镜技术,观察白杨派树种毛白杨、毛新杨、银腺杨、中国山杨花粉发育中生殖细胞的细胞质DNA及其在精细胞形成过程中的动态。结果表明:不同发育时期的生殖细胞、精细胞中不存在具有DNA的细胞器,为白杨派树种具有母系遗传的潜能提供了细胞学证据;其中,线粒体在花粉发育过程中一直存在,但其DNA发生了降解,从而使父系线粒体DNA的传递中断,导致了线粒体的母系遗传。细胞学观察发现,银腺杨少数质体及其DNA被排除和降解的时期相对迟缓。本文还对被子植物线粒体遗传的机理进行了讨论。 相似文献
4.
Burns KH Viveiros MM Ren Y Wang P DeMayo FJ Frail DE Eppig JJ Matzuk MM 《Science (New York, N.Y.)》2003,300(5619):633-636
Upon fertilization, remodeling of condensed maternal and paternal gamete DNA occurs to form the diploid genome. In Xenopus laevis, nucleoplasmin 2 (NPM2) decondenses sperm DNA in vitro. To study chromatin remodeling in vivo, we isolated mammalian NPM2 orthologs. Mouse NPM2 accumulates in oocyte nuclei and persists in preimplantation embryos. Npm2 knockout females have fertility defects owing to failed preimplantation embryo development. Although sperm DNA decondensation proceeds without NPM2, abnormalities are evident in oocyte and early embryonic nuclei. These defects include an absence of coalesced nucleolar structures and loss of heterochromatin and deacetylated histone H3 that normally circumscribe nucleoli in oocytes and early embryos, respectively. Thus, Npm2 is a maternal effect gene critical for nuclear and nucleolar organization and embryonic development. 相似文献
5.
Chromatin structure and de novo methylation of sperm DNA: implications for activation of the paternal genome 总被引：22，自引：0，他引：22
The chromatin structure characteristic of constitutively expressed genes, tissue-specific genes, and inactive genes is absent in chicken sperm chromatin. However, point sites of undermethylation in sperm DNA within constitutively expressed genes, but not within globin genes or an inactive gene, correspond to the location of regions of altered chromatin structure (hypersensitive sites) in somatic tissue and spermatogonial cells. A de novo methylation process whereby regions within and flanking these genes become methylated, but which excludes the methylation of sequences within hypersensitive sites, occurs between the spermatogonial stage and the first meiotic prophase. These undermethylated regions may play a role in the activation of the paternal genome during embryogenesis. 相似文献
6.
嫩度是决定肉食用品质的重要指标。宰后肉的嫩度发生不连续变化,严重降低了消费者的购买意愿,因此阐明宰后嫩化机理一直是肉品科学领域的研究热点。自“凋亡”的概念引入至宰后肌肉嫩化过程后一直广受关注,动物被屠宰放血后,活性氧（reactive oxygen species,ROS）大量累积,ATP（adenosine triphosphate）逐渐耗尽,必然导致细胞死亡。宰后肌细胞死亡和肌肉嫩化都是在一系列调控因子作用下激活肌肉内源酶,并由内源酶水解蛋白质破坏细胞结构,因此这两个生化过程被认为高度相关。本文综述了宰后肌细胞主要以凋亡的形式死亡,分析了除凋亡外,宰后早期产生少量ROS时细胞会通过自噬启动自身防御系统,宰后后期ATP逐渐耗尽肌细胞可能从凋亡转变为坏死;明确了线粒体通路是宰后肌肉中细胞凋亡酶激活的关键路径,线粒体死亡因子释放是细胞内死亡级联反应的总开关,其开放状态直接决定着细胞以何种途径进行死亡,并进一步从线粒体膜通透化和内膜嵴重构两方面,讨论了宰后线粒体损伤诱导凋亡因子的释放机理;综述了线粒体损伤变化及其对嫩化过程的影响,并从线粒体通过参与能量代谢影响肌肉pH以及通过释放凋亡因子调控细胞凋亡酶活性两方面分析了其潜在机理;探讨了宰后肌肉线粒体与内质网间相互作用以影响Ca2+信号传导以及细胞凋亡过程,或与溶酶体相互作用,破坏溶酶体膜稳定性,使其释放组织蛋白酶以激活线粒体Bax和Bid而加速线粒体膜通透性;综述了细胞凋亡酶在宰后早期被激活,并参与部分肌原纤维蛋白的有限降解,但随着宰后时间的延长,ATP逐渐耗尽等因素导致细胞凋亡酶失活,因此细胞凋亡酶只参与宰后早期的嫩化过程。综述内容可为完善宰后肌肉嫩化过程提供理论参考。 相似文献
7.
Protein sorting to mitochondria: evolutionary conservations of folding and assembly 总被引：57，自引：0，他引：57
According to the endosymbiont hypothesis, mitochondria have lost the autonomy of their prokaryotic ancestors. They have to import most of their proteins from the cytosol because the mitochondrial genome codes for only a small percentage of the polypeptides that reside in the organelle. Recent findings show that the sorting of proteins into the mitochondrial subcompartments and their folding and assembly follow principles already developed in prokaryotes. The components involved may have structural and functional equivalents in bacteria. 相似文献
8.
Ogawa M Yoshimori T Suzuki T Sagara H Mizushima N Sasakawa C 《Science (New York, N.Y.)》2005,307(5710):727-731
The degradation of undesirable cellular components or organelles, including invading microbes, by autophagy is crucial for cell survival. Here, Shigella, an invasive bacteria, was found to be able to escape autophagy by secreting IcsB by means of the type III secretion system. Mutant bacteria lacking IcsB were trapped by autophagy during multiplication within the host cells. IcsB did not directly inhibit autophagy. Rather, Shigella VirG, a protein required for intracellular actin-based motility, induced autophagy by binding to the autophagy protein, Atg5. In nonmutant Shigella, this binding is competitively inhibited by IcsB binding to VirG. 相似文献
9.
Yaffe MP 《Science (New York, N.Y.)》1999,283(5407):1493-1497
The distribution of mitochondria to daughter cells during cell division is an essential feature of cell proliferation. Until recently, it was commonly believed that inheritance of mitochondria and other organelles was a passive process, a consequence of their random diffusion throughout the cytoplasm. A growing recognition of the reticular morphology of mitochondria in many living cells, the association of mitochondria with the cytoskeleton, and the coordinated movements of mitochondria during cellular division and differentiation has illuminated the necessity for a cellular machinery that mediates mitochondrial behavior. Characterization of the underlying molecular components of this machinery is providing insight into mechanisms regulating mitochondrial morphology and distribution. 相似文献
10.
应用透射电镜技术研究了超低温冷冻保存对中间球海胆Strongylocentrotus intermedius精子超微结构的影响。结果表明：不加抗冻剂的情况下,精子线粒体和顶体结构不完整,质膜、鞭毛破损。加入保护剂后,多数精子结构完好,部分精子细胞器受损,表现为质膜褶皱或膨胀举起,与核膜的间隙明显增大;顶体肿胀、破裂或脱落;线粒体嵴间隙增大,内部出现空泡,甚至线粒体内膜破损,内嵴减少,呈弥散状;鞭毛被膜肿胀,呈波浪状,＂9＋2＂型结构模糊;细胞核结构没有明显变化。应用单细胞凝胶电泳技术研究了精子冷冻保存前后DNA的损伤。结果表明,不加抗冻剂的冷冻组及添加抗冻剂的试验组精子DNA损伤情况与鲜精相比均无显著差异（P〉0.05）,冷冻对精子结构的损伤是造成精子活力及受精率下降的主要原因。 相似文献
11.
Alterations of mitochondrial functions are linked to multiple degenerative or acute diseases. As mitochondria age in our cells, they become progressively inefficient and potentially toxic, and acute damage can trigger the permeabilization of mitochondrial membranes to initiate apoptosis or necrosis. Moreover, mitochondria have an important role in pro-inflammatory signaling. Autophagic turnover of cellular constituents, be it general or specific for mitochondria (mitophagy), eliminates dysfunctional or damaged mitochondria, thus counteracting degeneration, dampening inflammation, and preventing unwarranted cell loss. Decreased expression of genes that regulate autophagy or mitophagy can cause degenerative diseases in which deficient quality control results in inflammation and the death of cell populations. Thus, a combination of mitochondrial dysfunction and insufficient autophagy may contribute to multiple aging-associated pathologies. 相似文献
12.
B J Murphy E D Robin D P Tapper R J Wong D A Clayton 《Science (New York, N.Y.)》1984,223(4637):707-709
The effect of hypoxic exposure on various mitochondrial enzymes and on cell mitochondrial genomic content was studied in two types of mammalian cells. Hypoxia depressed the activity of six enzymes to the same degree. The kinetics of depression and of recovery during reexposure to normoxia were statistically similar for three marker enzymes. Despite the global and symmetrical decrease in enzyme activities, mitochondrial DNA remained constant. This suggests either symmetrical loss of mitochondrial enzymes from all mitochondria or complete loss of enzymes from a subpopulation of mitochondria with retention of an intact mitochondrial genome. 相似文献
13.
14.
Directing cell division during development 总被引：14，自引：0，他引：14
15.
Wei MC Zong WX Cheng EH Lindsten T Panoutsakopoulou V Ross AJ Roth KA MacGregor GR Thompson CB Korsmeyer SJ 《Science (New York, N.Y.)》2001,292(5517):727-730
Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of a "BH3-domain-only" BCL-2 family member, triggers the homooligomerization of "multidomain" conserved proapoptotic family members BAK or BAX, resulting in the release of cytochrome c from mitochondria. We find that cells lacking both Bax and Bak, but not cells lacking only one of these components, are completely resistant to tBID-induced cytochrome c release and apoptosis. Moreover, doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin. Thus, activation of a "multidomain" proapoptotic member, BAX or BAK, appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli. 相似文献
16.
Phosphorylation of ULK1 (hATG1) by AMP-activated protein kinase connects energy sensing to mitophagy
Egan DF Shackelford DB Mihaylova MM Gelino S Kohnz RA Mair W Vasquez DS Joshi A Gwinn DM Taylor R Asara JM Fitzpatrick J Dillin A Viollet B Kundu M Hansen M Shaw RJ 《Science (New York, N.Y.)》2011,331(6016):456-461
Adenosine monophosphate-activated protein kinase (AMPK) is a conserved sensor of intracellular energy activated in response to low nutrient availability and environmental stress. In a screen for conserved substrates of AMPK, we identified ULK1 and ULK2, mammalian orthologs of the yeast protein kinase Atg1, which is required for autophagy. Genetic analysis of AMPK or ULK1 in mammalian liver and Caenorhabditis elegans revealed a requirement for these kinases in autophagy. In mammals, loss of AMPK or ULK1 resulted in aberrant accumulation of the autophagy adaptor p62 and defective mitophagy. Reconstitution of ULK1-deficient cells with a mutant ULK1 that cannot be phosphorylated by AMPK revealed that such phosphorylation is required for mitochondrial homeostasis and cell survival during starvation. These findings uncover a conserved biochemical mechanism coupling nutrient status with autophagy and cell survival. 相似文献
17.
Fukami K Nakao K Inoue T Kataoka Y Kurokawa M Fissore RA Nakamura K Katsuki M Mikoshiba K Yoshida N Takenawa T 《Science (New York, N.Y.)》2001,292(5518):920-923
Several phospholipase C (PLC) isoforms have been found in male and female mammalian gametes, and splicing isoforms of PLCdelta4 are predominantly expressed in testis. Here we report that male mice in which the PLCdelta4 gene had been disrupted either produced few small litters or were sterile. In vitro fertilization studies showed that insemination with PLCdelta4-/- sperm resulted in significantly fewer eggs becoming activated and that the calcium transients associated with fertilization were absent or delayed. PLCdelta4-/- sperm were unable to initiate the acrosome reaction, an exocytotic event required for fertilization and induced by interaction with the egg coat, the zona pellucida. These data demonstrate that PLCdelta4 functions in the acrosome reaction that is induced by the zona pellucida during mammalian fertilization. 相似文献
18.
将１０例正常生育男性的精液标本进行冷冻保存、复温后电镜观察。结果,冷冻精子复温后精子超微结构发生了不同程度的改变,其主要改变为精子顶体肿胀,顶体内、外膜分离,外膜形成波浪状皱褶,有的核局部出现凹陷,线粒体改变呈基质密度降低,结构模糊等。但是,精子基本结构保持完整。研究结果表明：冷冻精子超微结构改变的主要原因是在冷冻过程中,由于冰晶形成的影响,水分内移,细胞肿胀,因而造成其活动率的明显下降。但并不影响授精能力。 相似文献
19.
Oocytes, the female germ cells, contain all the messenger RNAs necessary to start a new life but typically wait until fertilization to begin development. The transition from oocyte to fertilized egg (zygote) involves many changes, including protein synthesis, protein and RNA degradation, and organelle remodeling. These changes occur concurrently with the meiotic divisions that produce the haploid maternal genome. Accumulating evidence indicates that the cell-cycle regulators that control the meiotic divisions also regulate the many changes that accompany the oocyte-to-zygote transition. We suggest that the meiotic machinery functions as an internal pacemaker that propels oocytes toward embryogenesis. 相似文献
20.
A "selfish" B chromosome that enhances its transmission by eliminating the paternal genome 总被引：5，自引：0，他引：5
U Nur J H Werren D G Eickbush W D Burke T H Eickbush 《Science (New York, N.Y.)》1988,240(4851):512-514
In the parasitic wasp, Nasonia vitripennis, males are haploid and usually develop from unfertilized eggs, whereas females are diploid and develop from fertilized eggs. Some individuals in this species carry a genetic element, termed psr (paternal sex ratio), which is transmitted through sperm and causes condensation and subsequent loss of paternal chromosomes in fertilized eggs, thus converting diploid females into haploid males. In this report the psr trait was shown to be caused by a supernumerary chromosome. This B chromosome contains at least three repetitive DNA sequences that do not cross-hybridize to each other or to the host genome. The psr chromosome apparently produces a trans-acting product responsible for condensation of the paternal chromosomes, but is itself insensitive to the effect. Because the psr chromosome enhances its transmission by eliminating the rest of the genome, it can be considered the most "selfish" genetic element yet described. 相似文献