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1.
为解析多倍体植物减数分裂期同源染色体的正常配对和联会的细胞学机制,以白菜同源多倍体为研究对象,利用免疫荧光分析技术,解析了联会复合体相关蛋白ZYP1在减数分裂前期I过程中的细胞学行为。结果表明:与二倍体相比,白菜同源多倍体减数分裂期同源染色体联会、配对及分离过程基本正常,联会复合体蛋白ZYP1抗体荧光信号变化趋势基本一致,但ZYP1免疫荧光信号显著增强。因此,与二倍体相比,同源多倍体植物很可能通过增强联会复合体蛋白ZYP1的表达水平,以协调同源染色体的正常联会与配对,进而保证多倍体植物的正常减数分裂过程。 相似文献
2.
Pawlowski WP Golubovskaya IN Timofejeva L Meeley RB Sheridan WF Cande WZ 《Science (New York, N.Y.)》2004,303(5654):89-92
Pairing, synapsis, and recombination are prerequisites for accurate chromosome segregation in meiosis. The phs1 gene in maize is required for pairing to occur between homologous chromosomes. In the phs1 mutant, homologous chromosome synapsis is completely replaced by synapsis between nonhomologous partners. The phs1 gene is also required for installation of the meiotic recombination machinery on chromosomes, as the mutant almost completely lacks chromosomal foci of the recombination protein RAD51. Thus, in the phs1 mutant, synapsis is uncoupled from recombination and pairing. The protein encoded by the phs1 gene likely acts in a multistep process to coordinate pairing, recombination, and synapsis. 相似文献
3.
Faithful chromosome segregation and repair of DNA double-strand breaks (DSBs) require cohesin, the protein complex that mediates sister-chromatid cohesion. Cohesion between sister chromatids is thought to be generated only during ongoing DNA replication by an obligate coupling between cohesion establishment factors such as Eco1 (Ctf7) and the replisome. Using budding yeast, we challenge this model by showing that cohesion is generated by an Eco1-dependent but replication-independent mechanism in response to DSBs in G(2)/M. Furthermore, our studies reveal that Eco1 has two functions: a cohesive activity and a conserved acetyltransferase activity, which triggers the generation of cohesion in response to the DSB and the DNA damage checkpoint. Finally, the DSB-induced cohesion is not limited to broken chromosomes but occurs also on unbroken chromosomes, suggesting that the DNA damage checkpoint through Eco1 provides genome-wide protection of chromosome integrity. 相似文献
4.
Checkpoints are evolutionarily conserved signaling mechanisms that arrest cell division and alter cellular stress resistance in response to DNA damage or stalled replication forks. To study the consequences of loss of checkpoint functions in whole animals, checkpoint genes were inactivated in the nematode C. elegans. We show that checkpoint proteins are not only essential for normal development but also determine adult somatic maintenance. Checkpoint proteins play a role in the survival of postmitotic adult cells. 相似文献
5.
In response to environmental signals such as anoxia, many organisms enter a state of suspended animation, an extreme form of quiescence in which microscopically visible movement ceases. We have identified a gene, san-1, that is required for suspended animation in Caenorhabditis elegans embryos. We show that san-1 functions as a spindle checkpoint component in C. elegans. During anoxia-induced suspended animation, embryos lacking functional SAN-1 or a second spindle checkpoint component, MDF-2, failed to arrest the cell cycle, exhibited chromosome missegregation, and showed reduced viability. These data provide a model for how a dynamic biological process is arrested in suspended animation. 相似文献
6.
Palframan WJ Meehl JB Jaspersen SL Winey M Murray AW 《Science (New York, N.Y.)》2006,313(5787):680-684
The spindle checkpoint delays cell cycle progression until microtubules attach each pair of sister chromosomes to opposite poles of the mitotic spindle. Following sister chromatid separation, however, the checkpoint ignores chromosomes whose kinetochores are attached to only one spindle pole, a state that activates the checkpoint prior to metaphase. We demonstrate that, in budding yeast, mutual inhibition between the anaphase-promoting complex (APC) and Mps1, an essential component of the checkpoint, leads to sustained inactivation of the spindle checkpoint. Mps1 protein abundance decreases in anaphase, and Mps1 is a target of the APC. Furthermore, expression of Mps1 in anaphase, or repression of the APC in anaphase, reactivates the spindle checkpoint. This APC-Mps1 feedback circuit allows cells to irreversibly inactivate the checkpoint during anaphase. 相似文献
7.
The Maternal-Effect Sterile (MES) proteins are essential for germline viability in Caenorhabditis elegans. Here, we report that MES-4, a SET-domain protein, binds to the autosomes but not to the X chromosomes. MES-2, MES-3, and MES-6 are required to exclude MES-4 and markers of active chromatin from the X chromosomes. These findings strengthen the emerging view that in the C. elegans germ line, the X chromosomes differ in chromatin state from the autosomes and are generally silenced. We propose that all four MES proteins participate in X-chromosome silencing, and that the role of MES-4 is to exclude repressors from the autosomes, thus enabling efficient repression of the Xs. 相似文献
8.
Crackower MA Kolas NK Noguchi J Sarao R Kikuchi K Kaneko H Kobayashi E Kawai Y Kozieradzki I Landers R Mo R Hui CC Nieves E Cohen PE Osborne LR Wada T Kunieda T Moens PB Penninger JM 《Science (New York, N.Y.)》2003,300(5623):1291-1295
Meiosis is a critical stage of gametogenesis in which alignment and synapsis of chromosomal pairs occur, allowing for the recombination of maternal and paternal genomes. Here we show that FK506 binding protein (Fkbp6) localizes to meiotic chromosome cores and regions of homologous chromosome synapsis. Targeted inactivation of Fkbp6 in mice results in aspermic males and the absence of normal pachytene spermatocytes. Moreover, we identified the deletion of Fkbp6 exon 8 as the causative mutation in spontaneously male sterile as/as mutant rats. Loss of Fkbp6 results in abnormal pairing and misalignments between homologous chromosomes, nonhomologous partner switches, and autosynapsis of X chromosome cores in meiotic spermatocytes. Fertility and meiosis are normal in Fkbp6 mutant females. Thus, Fkbp6 is a component of the synaptonemal complex essential for sex-specific fertility and for the fidelity of homologous chromosome pairing in meiosis. 相似文献
9.
The spindle checkpoint was characterized in meiosis of budding yeast. In the absence of the checkpoint, the frequency of meiosis I missegregation increased with increasing chromosome length, reaching 19% for the longest chromosome. Meiosis I nondisjunction in spindle checkpoint mutants could be prevented by delaying the onset of anaphase. In a recombination-defective mutant (spo11Delta), the checkpoint delays the biochemical events of anaphase I, suggesting that chromosomes that are attached to microtubules but are not under tension can activate the spindle checkpoint. Spindle checkpoint mutants reduce the accuracy of chromosome segregation in meiosis I much more than that in meiosis II, suggesting that checkpoint defects may contribute to Down syndrome. 相似文献
10.
本文报道了分布于我国云南中部的中国雉鸡(Phasianus colchicus)的染色体组型、G-带及高分辨G-带带型。染色体数目2n=82。性染色体雄性为ZZ、雌性为ZW。40对常染色体中,1号为近中着丝粒染色体,5号为近端着丝粒染色体,其余皆为端部着丝粒染色体;性染色体Z为中着丝粒染色体,W为近端着丝粒染色体。全部染色体进行测量分析,计算相对长度和双臂染色体着丝粒指数。根据相对长度和着丝粒指数,绘制了染色体组模式图。制作了1—20号常染色体和性染色体Z的中期G-带以及全部染色体的高分辨G-带,并进行了两种G-带带型特征的描述和比较,绘制了两种G-带比较模式图。 相似文献
11.
八倍体节节麦-燕麦部分双二倍体的细胞遗传学鉴定 总被引：3，自引：0，他引：3
通过对节节麦、野燕麦、八倍体节节麦－燕麦部分双二倍体的Ｃ分带的研究,表明八倍体节节麦－燕麦部分双二倍体中含有小麦的Ｂ组和Ａ组染色体。通过对节节麦、野燕麦、八倍体节节麦－燕麦部分双二倍体与中国春小麦回交后代的花粉母细胞减数分裂过程中染色体配对行为的研究,表明回交一代中含有１４个左右的二价体,而不是预期的７个二价体;通过对八倍体节节麦－燕麦部分双二倍体与中国春小麦回交后代花粉母细胞中染色体的原位杂交研究,表明八倍体节节麦－燕麦部分双二倍体中含有１４条左右的燕麦染色体。因此,认为八倍体节节麦－燕麦部分双二倍体不是真正的节节麦与野燕麦的杂种,而可能是某一四倍体小麦与燕麦的杂交后代。 相似文献
12.
Reproductive cells that are destined to become sperm or egg undergo meiotic division during which the chromosome number is halved. As Sluder and McCollum explain in their Perspective, new findings (Shonn et al.) in yeast show that there is a spindle checkpoint that operates during meiosis to ensure that an equal number of replicated chromosomes arrives at each pole of the cell. One of the components of this meiotic spindle checkpoint turns out to be Mad2, which gives the signal to halt meiosis if it looks like unequal chromosome segregation is taking place. 相似文献
13.
Coordination of cytokinesis with chromosome congression and segregation is critical for proper cell division, but the mechanism is unknown. Here, septins, a conserved family of polymerizing guanosine triphosphate-binding proteins, localized to the metaphase plate during mitosis. Septin depletion resulted in chromosome loss from the metaphase plate, lack of chromosome segregation and spindle elongation, and incomplete cytokinesis upon delayed mitotic exit. These defects correlated with loss of the mitotic motor and the checkpoint regulator centromere-associated protein E (CENP-E) from the kinetochores of congressing chromosomes. Mammalian septins may thus form a mitotic scaffold for CENP-E and other effectors to coordinate cytokinesis with chromosome congression and segregation. 相似文献
14.
We describe a process in meiotic cells of budding yeast in which chromosomes become joined together in pairs at their centromeres independent of chromosomal homology. These centromeric interactions depend on the synaptonemal complex component Zip1. During meiosis in wild-type diploids, centromere couples are initially nonhomologous and then undergo switching until all couples involve homologs. This transition to homologous coupling depends on Spo11, a protein required for the initiation of meiotic recombination. Regions of synaptonemal complex assembled early in meiosis are often centromere-associated. We propose that centromere coupling facilitates homolog pairing and promotes synapsis initiation. 相似文献
15.
Taylor SS Hardwick KG Sawin KE Biggins S Piatti S Khodjakov A Rieder CL Salmon ED Musacchio A 《Science (New York, N.Y.)》2007,316(5827):982; author reply 982
Müller et al. (Reports, 27 October 2006, p. 654) proposed a role for microtubule nucleation in mitotic checkpoint signaling. However, their observations of spindle defects and mitotic delay after depletion of gamma-tubulin ring complex (gamma-TuRC) components are fully consistent with activation of the established pathway of checkpoint signaling in response to incomplete or unstable interactions between kinetochores of mitotic chromosomes and spindle microtubules. 相似文献
16.
The spindle checkpoint delays sister chromatid separation until all chromosomes have undergone bipolar spindle attachment. Checkpoint failure may result in chromosome mis-segregation and may contribute to tumorigenesis. We showed that the human protein Hec1 was required for the recruitment of Mps1 kinase and Mad1/Mad2 complexes to kinetochores. Depletion of Hec1 impaired chromosome congression and caused persistent activation of the spindle checkpoint, indicating that high steady-state levels of Mad1/Mad2 complexes at kinetochores were not essential for checkpoint signaling. Simultaneous depletion of Hec1 and Mad2 caused catastrophic mitotic exit, making Hec1 an attractive target for the selective elimination of spindle checkpoint-deficient cells. 相似文献
17.
Brissett NC Pitcher RS Juarez R Picher AJ Green AJ Dafforn TR Fox GC Blanco L Doherty AJ 《Science (New York, N.Y.)》2007,318(5849):456-459
Nonhomologous end joining (NHEJ) is a critical DNA double-strand break (DSB) repair pathway required to maintain genome stability. Many prokaryotes possess a minimalist NHEJ apparatus required to repair DSBs during stationary phase, composed of two conserved core proteins, Ku and ligase D (LigD). The crystal structure of Mycobacterium tuberculosis polymerase domain of LigD mediating the synapsis of two noncomplementary DNA ends revealed a variety of interactions, including microhomology base pairing, mismatched and flipped-out bases, and 3' termini forming hairpin-like ends. Biochemical and biophysical studies confirmed that polymerase-induced end synapsis also occurs in solution. We propose that this DNA synaptic structure reflects an intermediate bridging stage of the NHEJ process, before end processing and ligation, with both the polymerase and the DNA sequence playing pivotal roles in determining the sequential order of synapsis and remodeling before end joining. 相似文献
18.
Fork reversal and ssDNA accumulation at stalled replication forks owing to checkpoint defects 总被引：1，自引：0，他引：1
Checkpoint-mediated control of replicating chromosomes is essential for preventing cancer. In yeast, Rad53 kinase protects stalled replication forks from pathological rearrangements. To characterize the mechanisms controlling fork integrity, we analyzed replication intermediates formed in response to replication blocks using electron microscopy. At the forks, wild-type cells accumulate short single-stranded regions, which likely causes checkpoint activation, whereas rad53 mutants exhibit extensive single-stranded gaps and hemi-replicated intermediates, consistent with a lagging-strand synthesis defect. Further, rad53 cells accumulate Holliday junctions through fork reversal. We speculate that, in checkpoint mutants, abnormal replication intermediates begin to form because of uncoordinated replication and are further processed by unscheduled recombination pathways, causing genome instability. 相似文献
19.
Although broken chromosomes can induce apoptosis, natural chromosome ends (telomeres) do not trigger this response. It is shown that this suppression of apoptosis involves the telomeric-repeat binding factor 2 (TRF2). Inhibition of TRF2 resulted in apoptosis in a subset of mammalian cell types. The response was mediated by p53 and the ATM (ataxia telangiectasia mutated) kinase, consistent with activation of a DNA damage checkpoint. Apoptosis was not due to rupture of dicentric chromosomes formed by end-to-end fusion, indicating that telomeres lacking TRF2 directly signal apoptosis, possibly because they resemble damaged DNA. Thus, in some cells, telomere shortening may signal cell death rather than senescence. 相似文献
20.
叶自行 《华南农业大学学报》1991,12(2):48-55
经辐射处理的甜橙花粉母细胞减数分裂中出现染色体易位、倒位、不联会的单价体等异常现象。由此而引成的花粉形态出现各种变异,育性降低,因而产生无籽少籽的果实。经统计分析,染色体畸变的细胞频率与果实的种子数为显著的负相关,花粉发芽率与果实的种子数为显著的正相关。在各种染色体异常中,不联会的单价体是引起花粉败育产生无籽果实的主要原因。 相似文献