2012年《遗传》第12期封面说明

蝗虫材料易得,染色体大,染色体数目相对较少,双线期和终变期交叉明显,可以用于分析染色体交叉的结构、分布和频率,是观察减数分裂过程中染色体动态变化的理想材料。在蝗虫的曲细精管中同时存在精子发生的3个过程,即精原细胞有丝分裂,初/次级精母细胞减数分裂及精子形成。     

减数分裂实验材料的优化与染色体制备技术改进

“优化”的实验材料是遗传学实验教学达到预期目标的必备条件之一,蝗虫精子形成中的减数分裂是比较好的观察减数分裂的材料之一。分别从蝗虫品种、捕捉时间、精细管取材位置等方面优化实验材料,同时通过改进染色技术提高染色体制片效果,有利于学生更有效地理解减数分裂的概念以及各个分裂时期染色体特征,牢固掌握遗传学基本定律。     

2种短翅型蝗虫减数分裂比较研究

减数分裂是生物有性繁殖过程中产生配子的一种特殊分裂方式,其过程中染色体行为在一定程度上反映物种的产生、分化和演变。对2种云南分布的短翅型蝗虫减数分裂中染色体行为特征进行研究,结果显示:两者减数分裂各个时期的特征基本一致,但双线期、终变期存在显著差异,二齿龙川蝗同源染色体联会配对较曲尾龙川蝗更为复杂。     

蝗虫减数分裂的观察

观察减数分裂的材料很多。在动物材料中,蝗虫精子形成中的减数分裂是比较好的材料。蝗虫染色体数目较少(雄性2n=23,×0;雌性2n=24,××),染色体较大,易于观察。在同一玻片标本上能同时观察减数分裂各期的染色体,还可观察有丝分裂过程及精子的变态过程。其方法简介如下: (一)取材蝗虫雌雄个体易于区别,一般雄体成虫较小,其腹部末端如船尾状,雌体较大,腹部末端分叉。捕捉成体雄蝗,活体取其精巢。先将翅及附肢从基部剪去,沿腹     

雄性东亚钳蝎减数分裂和染色体组型

本文作者对我国药用动物东亚钳蝎——Buthusmartensi的精母细胞减数分裂和染色体组型进行初步观察。该虫的减数分裂有细线期、偶线期、粗线期、双线期和终变期。染色体数目24者居多,2n=24,即2n=22A+xy。染色体组型有3对为中部着丝粒染色体,7对亚中部着丝粒和1对端部着丝粒染色体。1对性染色体xy均为亚中部着丝粒染色体。     

一个精原细胞形成几个精子

有人对初级精母细胞有没有染色体复制持否定意见,认为精原细胞经过染色体复制以后才转变为初级精母细胞。有关资料对此叙述模糊不清,因此有必要澄清。睾丸的曲细精管是产生精子的地方。曲细精管内生精上皮产生精子的过程是:精原细胞不断进行有丝分裂,增加细胞数量,产生形态特征和分化程度不同的精原细胞,直至分裂、长大分化成为初级精母细胞。初级精母细胞经过减数分裂第一次分裂的间期生长和染色体复制后分裂为两个次级精母细胞(染色体数目减半)。每个次级精母细胞不经过生长     

小鼠卵母细胞减数分裂染色体的简易制备

正常的减数分裂是有性生殖的前提,它保证了上下代之间染色体结构和数目的稳定性。几乎所有的核型异常都来自减数分裂过程中的错误,这些错误包括同源染色体不配对、染色体不分离(首次和二次不分离)、染色体结构畸变等。卵母细胞减数分裂过程中存在着两次停滞期,其中第一次停滞期长达几个月至几年甚至几十年。在此期间卵母细胞受环境或自身病变的影响,极容易发生染色体畸变。有报道表明,卵母细胞比精母细胞在减数分裂过程中更容易发生错误。     

小鼠精母细胞性染色体的观察

精母细胞减数分裂的研究是细胞遗传学中 的重要领域。虽然早就确立了减数分裂染色体 减半的原理,但由于精母细胞或卵母细胞都呈 组织状态,从中取出减数分裂的细胞进行染色 体研究并不容易。因此,对减数分裂过程中染 色体形态变化的研究,在相当长的历史时期里 停滞不前。六十年代以来,由于在制片方法上 的改进和各种新技术的应用,使体细胞染色体 的研究有了飞速的发展,也为进一步研究生殖 细胞染色体开创了新的途径。     

组蛋白H3Ser10磷酸化在家蚕精母细胞减数分裂中的动态分布

【目的】探究组蛋白H3Ser10磷酸化(H3Ser10ph)在家蚕Bombyx mori精母细胞减数分裂中的功能。【方法】解剖并分离家蚕4龄幼虫至蛹期精巢组织,通过丙烯酰胺凝胶包埋制备处于减数分裂不同时期的精巢组织玻片,以免疫荧光标记检测H3Ser10ph抗体在精母细胞减数分裂不同时期的定位特点。【结果】在家蚕有核精子精母细胞减数分裂过程中,组蛋白H3Ser10的磷酸化发生在粗线期染色体的特定位置,双线期H3Ser10ph信号逐渐减弱,至终变期时在染色体上完全检测不到磷酸化信号。随着细胞周期的进行,磷酸化信号又开始逐渐增强,减数第一次分裂中期时达到最高水平。当细胞进入减数第二次分裂前中期时,染色体臂上的H3Ser10ph信号消失,在靠近纺锤体微管的分裂面处有弥散的H3Ser10ph抗体的信号,减数第二次分裂末期,仅剩余非常微弱的H3Ser10ph信号残留于染色体的特定位置。在无核精子精母细胞减数分裂过程中,在中期I至末期I一直在染色体上有较均一的3Ser10ph信号,后期I时纺锤丝微管与赤道面平行。【结论】组蛋白H3Ser10磷酸化与家蚕有核精子和无核精子精母细胞减数分裂中染色质的动态变化相关。     

四倍体鲫鲤、三倍体湘云鲫染色体减数分裂观察

用精巢细胞直接制片法观察了异源四倍体鲫鲤、三倍体湘云鲫和二倍体红鲫、湘江野鲤精母细胞染色体第一次减数分裂中期配对情况 ;作为对照 ,观察了上述四种鱼肾细胞的有丝分裂中期染色体。在精母细胞第一次减数分裂中 ,异源四倍体鲫鲤同源染色体两两配对 ,形成 10 0个二价体 ,没有观察到单价体、三价体和四价体 ;三倍体湘云鲫精母细胞形成 5 0个二价体和 5 0个单价体 ;红鲫和湘江野鲤精母细胞分别形成 5 0个二价体。肾细胞检测表明异源四倍体的染色体数目为 4n =2 0 0 ;湘云鲫为 3n =15 0 ;红鲫和湘江野鲤分别为 2n =10 0。减数分裂时染色体分布情况与肾细胞染色体检测结果相吻合。具有四套染色体的异源四倍体鲫鲤在减数分裂中只形成 10 0个二价体 ,而不形成 2 5个四价体或其它形式 ,为产生稳定一致的二倍体配子提供了重要的遗传保障 ,也为人工培育的异源四倍体鲫鲤群体能够世世代代自身繁衍下去提供了重要的遗传学证据。三倍体湘云鲫在减数分裂过程中出现二价体、单价体共存 ,同源染色体在配对和分离中出现紊乱 ,导致非整倍体生殖细胞的产生 ,为湘云鲫的不育性提供了染色体水平上的证据     

SUN1 is required for telomere attachment to nuclear envelope and gametogenesis in mice

Prior to the pairing and recombination between homologous chromosomes during meiosis, telomeres attach to the nuclear envelope and form a transient cluster. However, the protein factors mediating meiotic telomere attachment to the nuclear envelope and the requirement of this attachment for homolog pairing and synapsis have not been determined in animals. Here we show that the inner nuclear membrane protein SUN1 specifically associates with telomeres between the leptotene and diplotene stages during meiotic prophase I. Disruption of Sun1 in mice prevents telomere attachment to the nuclear envelope, efficient homolog pairing, and synapsis formation in meiosis. Massive apoptotic events are induced in the mutant gonads, leading to the abolishment of both spermatogenesis and oogenesis. This study provides genetic evidence that SUN1-telomere interaction is essential for telomere dynamic movement and is required for efficient homologous chromosome pairing/synapsis during mammalian gametogenesis.     

Lack of Checkpoint Control at the Metaphase/Anaphase Transition: A Mechanism of Meiotic Nondisjunction in Mammalian Females

A checkpoint mechanism operates at the metaphase/anaphase transition to ensure that a bipolar spindle is formed and that all the chromosomes are aligned at the spindle equator before anaphase is initiated. Since mistakes in the segregation of chromosomes during meiosis have particularly disastrous consequences, it seems likely that the meiotic cell division would be characterized by a stringent metaphase/ anaphase checkpoint. To determine if the presence of an unaligned chromosome activates the checkpoint and delays anaphase onset during mammalian female meiosis, we investigated meiotic cell cycle progression in murine oocytes from XO females and control siblings. Despite the fact that the X chromosome failed to align at metaphase in a significant proportion of cells, we were unable to detect a delay in anaphase onset. Based on studies of cell cycle kinetics, the behavior and segregation of the X chromosome, and the aberrant behavior and segregation of autosomal chromosomes in oocytes from XO females, we conclude that mammalian female meiosis lacks chromosome-mediated checkpoint control. The lack of this control mechanism provides a biological explanation for the high incidence of meiotic nondisjunction in the human female. Furthermore, since available evidence suggests that a stringent checkpoint mechanism operates during male meiosis, the lack of a comparable checkpoint in females provides a reason for the difference in the error rate between oogenesis and spermatogenesis.     

Budding yeast PDS5 plays an important role in meiosis and is required for sister chromatid cohesion

Budding yeast PDS5 is an essential gene in mitosis and is required for chromosome condensation and sister chromatid cohesion. Here we report that PDS also is required in meiosis. Pds5p localizes on chromosomes at all stages during meiotic cycle, except anaphase I. PDS5 plays an important role at first meiotic prophase. Failure in function of PDS5 causes premature separation of chromosomes. The loading of Pds5p onto chromosome requires the function of REC8, but the association of Rec8p with chromosome is independent of PDS5. Mutant analysis and live cell imaging indicate that PDS5 play a role in meiosis II as well.     

A link between meiotic prophase progression and crossover control

During meiosis, most organisms ensure that homologous chromosomes undergo at least one exchange of DNA, or crossover, to link chromosomes together and accomplish proper segregation. How each chromosome receives a minimum of one crossover is unknown. During early meiosis in Caenorhabditis elegans and many other species, chromosomes adopt a polarized organization within the nucleus, which normally disappears upon completion of homolog synapsis. Mutations that impair synapsis even between a single pair of chromosomes in C. elegans delay this nuclear reorganization. We quantified this delay by developing a classification scheme for discrete stages of meiosis. Immunofluorescence localization of RAD-51 protein revealed that delayed meiotic cells also contained persistent recombination intermediates. Through genetic analysis, we found that this cytological delay in meiotic progression requires double-strand breaks and the function of the crossover-promoting heteroduplex HIM-14 (Msh4) and MSH-5. Failure of X chromosome synapsis also resulted in impaired crossover control on autosomes, which may result from greater numbers and persistence of recombination intermediates in the delayed nuclei. We conclude that maturation of recombination events on chromosomes promotes meiotic progression, and is coupled to the regulation of crossover number and placement. Our results have broad implications for the interpretation of meiotic mutants, as we have shown that asynapsis of a single chromosome pair can exert global effects on meiotic progression and recombination frequency.     

Meiotic sex chromosome inactivation

X chromosome inactivation is most commonly studied in the context of female mammalian development, where it performs an essential role in dosage compensation. However, another form of X-inactivation takes place in the male, during spermatogenesis, as germ cells enter meiosis. This second form of X-inactivation, called meiotic sex chromosome inactivation (MSCI) has emerged as a novel paradigm for studying the epigenetic regulation of gene expression. New studies have revealed that MSCI is a special example of a more general mechanism called meiotic silencing of unsynapsed chromatin (MSUC), which silences chromosomes that fail to pair with their homologous partners and, in doing so, may protect against aneuploidy in subsequent generations. Furthermore, failure in MSCI is emerging as an important etiological factor in meiotic sterility.     

Aberrant spermatogenesis and the peculiar mechanism of sex determination in Symphypleonan Collembola (Insecta)

Light and electron microscopy evidence have been obtained to describe the peculiar spermatogenesis in the collembolan species Sminthurus viridis and Allacma fusca (Sminthuridae). In these two species, the two sexes differ for the lack of two chromosomes (the sex chromosomes) in males (males, 2n = 10; females, 2n = 12). While oogenesis seems to proceed normally, spermatogenesis is peculiar because the two daughter cells of the first meiotic division have different chromosome numbers (six and four). The cell receiving four chromosomes degenerates, while the cell receiving six chromosomes completes meiosis and produces identical spermatozoa (n = 6). At fertilization, pronuclei with six chromosomes fuse together to form zygotes with 2n = 12. Male embryos must lose two sex chromosomes during the first zygotic mitosis, as all male cells have 2n = 10 chromosomes. The sex chromosome system of these species can be identified as X1X1X2X2:X1X20. Electron microscopy observations show that the same peculiar spermatogenesis occurs also in two others species of the same family, Caprainea marginata and Lipothrix lubbocki. The peculiar sex determination system described is similar but not identical to what is observed in other insect orders, and it may represent an evolutionary step toward parthenogenesis. It is suggested that this peculiar spermatogenesis is common to all Symphypleona.