星豹蛛Pardos astigera染色体组型分析

首次报告星豹蛛的染色体形态结构,数目和性染色体组成,实验结果表明,星豹蛛染色体数目为：雄体２ｎ＝２８,雌体２ｎ＝３０,性别决定机制属于Ｘ１Ｘ２Ｏ型,Ｘ１为全部染色体中最长的,Ｘ２为全部染色体中最短的,全部染色体均为端着丝粒,这个结论可以被Ｃ－带标本所证实,且Ｃ－带带纹大小及染色深浅均无明显差异,Ｇ－带处理得到了稳定的,有重复性的带纹。     

迷宫漏斗蛛Aglena labyrinthica的染色体（蜘蛛目：漏斗蛛科）

报告迷宫漏斗蛛的染色体数目,形态结构和性染色体组成,结果表明,迷宫漏斗蛛体细胞染色体数目是：雄性２ｎ＝４２,雌性２ｎ＝４４,性别决定机制属Ｘ１Ｘ２Ｏ型,Ｘ染色体是全部染色体中最长的和最短的２个（对）,染色体似乎均为端或亚端着丝粒染色体,这由Ｃ－显带标本分析所证实,没有亚中着丝粒染色体的证据,Ｃ－带标本分析表明,常染色体中,各条染色全的Ｃ－带纹,其大小和染色深浅无明显差异,但Ｘ２染色体上有明显宽的Ｃ     

温室希蛛染色体的观察（蜘蛛目：珠蛛科）

报道了温室希蛛的染色体数目,形态结构和性染色体组成,从目前的结果可见,温室希蛛的染色体数目是,雄性体细胞染色体数为２ｎ＝２２,雌性为２ｎ＝２４其性决定机制属于Ｘ１Ｘ２Ｏ型,所有染色体似乎均为端或亚端着丝粒染色体,这个结论被其对Ｃ－带标本的分析所证实,两个（对）Ｘ－染色体是最短的和次最短的,温室希蛛染色体Ｃ－带标本的分析没有观察到染色体间有明显的结构差异,在染色体Ｇ－带标本中,获得了稳定的带纹。     

悦目金蛛(Argiope amoena)染色体的观察

对悦目金株（Ａｒｇｉｏｐｅ ａｍｏｅｎａ）染色体的数目、形态特征和性染色体组成,进行了核型分析,本实验观察胚胎细胞有丝分裂的Ｃ－中期相,悦目金蛛体细胞染色体数目是：雌性２ｎ＝２６,雄性２ｎ＝２４,性别决定机制属于ＸＸＯ型。     

白额巨蟹蛛（Heteropoda venatoria）染色体的初步观察

对白额巨蟹蛛的血细胞染色体进行初步研究,发现其雌蛛的体细胞染色体２ｎ＝４４,其中含有中部着丝粒染色体,亚中部着丝粒染色体和近端着丝粒染色体。     

三叶木通染色体组型研究

用ＡＳＧ法对三叶木通（Ａｋｅｂｉａ ｔｒｉｆｏｌｉａｔａ）根、茎尖细胞进行染色体制片,探讨其染色体组型。结果表明：三叶木通核型为２ｎ＝２Ｘ＝１６＝１０Ｍ＋２ＳＭ＋２ＳＴ＋２Ｔ,Ｘ＝８;２Ｂ类型,第２号染色体上有一对随体。三叶木通细胞中存在有混倍性现象,实生苗中２ｎ＝４Ｘ＝３２的四倍性细胞占７．９％;秋水仙素诱变苗、根茎占３１．８％～３７．９％。     

四种蚤染色体组型及C分带研究

本文首次在国内报道了住鼠客蚤、猫栉首蚤指名亚种、人蚤和秃病蚤蒙翼亚种的染色体组型和Ｃ分带研究结果。１、印鼠客蚤２ｎ＝１８＝１０ｍ＋６ｓｍ＋２ｓｔ,ＸＸ／ＹＹ．２猫蚤２ｎ＝１２＝１０ｍ＋２ｓｍ,ＸＸ／ＹＹ,核型特点为２号染色体的多态性和３号与６号染色体间发生不对称性易位。３、人蚤核型特点是：（１）染色体数目多态现象,变异范围８－１２,以９－１２者多见,ＸＸ／ＹＹ性染色体决定机制。（２）染色体结构重组     

中国西部高山8种龙胆属植物的染色体数目

本文报道了我国西部高山上的８种龙胆属植物的染色体数目。其中宽筒龙胆的染色体数目为２ｎ＝４８,提钟龙胆的染色体数目为２ｎ＝２６,小齿龙胆和四数龙胆的染色体数目为２ｎ＝２４,南山龙胆的染色体数目为２ｎ＝１８,上述５种植物的染色体数目为首次报道,其余蓝玉簪龙胆的染色体数目为２ｎ＝２４,线叶龙胆的染色体数目为２ｎ＝４８,钻叶龙胆的染色体数目为２ｎ＝１８。     

辽宁地区产6种乌头的细胞分类学研究

对我国辽宁地区毛莨科乌头属６个种的染色体的数目和形态进行了研究,并进行了核型分析。其染色体基数为Ｘ＝８,核型公式为：两色乌头：２ｎ＝２ｘ＝２ｍ＋１０ｓｍ＋４ｓｔ;蛇岛乌头为：２ｎ＝４ｘ＝１０ｍ＋２０ｓｍ（ＳＡＴ）＋２ｓｔ＋２Ｂ;黄花乌头为：２ｎ＝４ｘ＝４ｍ＋１２ｓｍ（ＳＡＴ）＋８ｓｔ＋１Ｂ;北乌头三倍体为：２ｎ＝３ｘ＝２Ｍ＋４ｍ＋１８ｓｍ;北乌头４倍体为２ｎ＝４ｘ＝４ｍ＋２８ｓｍ。同时,对乌头属下     

七种药用植物的染色体研究

对山东７种药用植物的染色体进行了研究。结果表明：田旋花（ＣｏｎｖｏｌｖｕｌｕｓａｒｖｅｎｓｉｓＬ）的染色体数目为２ｎ＝７８;蜜柑草（ＰｈｙｌａｎｔｈｕｓｍａｔｓｕｍｕｒａｅＨａｖａｔａ）的染色体数目为ｎ＝８８;挂红灯（ＰｈｙｓａｌｉｓａｌｋｅｋｅｎｇｉＬｖａｒｆｒａｎｃｈｅｔｉ（Ｍａｓｔ）Ｍａｋｉｎｏ）的染色体数目为２ｎ＝２４,核型公式为Ｋ（２ｎ）＝２４＝２ｍ＋１８ｓｍ＋２ｓｔ＋２ｓｔ（ｓａｔ）,核型“２Ａ”型;无剌曼陀罗（ＤａｔｕｒａｓｔｒａｍｏｎｉｕｍＬｖａｒｉｎｅｒｍｉｓ（Ｊａｃｑ）ＳｃｈｉｎｚｅｔＴｈｅｌ）的染色体数目为２ｎ＝２４,核型公式为Ｋ（２ｎ）＝２４＝２０ｍ＋４ｓｍ,核型“１Ｂ”型;决明（ＣａｓｉａｔｏｒａＬ）的染色体数目为２ｎ＝２６,核型公式为Ｋ（２ｎ）＝２６＝２４ｍ＋２ｓｍ,核型“１Ａ”型;荔枝草（ＳａｌｖｉａｐｌｅｂｅｉａＲＢｒ）的染色体数目为２ｎ＝１６,核型公式为Ｋ（２ｎ）＝１６＝６ｍ＋１０ｓｍ,核型“２Ａ”型;车前（ＰｌａｎｔａｇｏａｓｉａｔｉｃａＬ）的染色体数目为２ｎ＝３６,核型公式为Ｋ（２ｎ）＝３６＝３２ｍ＋４ｓｍ,核型“１Ａ”型。     

Transformation of Hprt gene with sperm DNA

Inactivation of the X chromosome during mammalian spermatogenesis has been postulated to occur by the same mechanism that controls female somatic X chromosome inactivation. We have used DNA-mediated transformation of HPRT- cells to test this idea, because it has been shown previously that inactive X chromosome DNA from somatic cells will not transform HPRT- cells. Isolated DNA from the mature sperm of five mammals (human, mouse, horse, bull, rabbit) were all capable of HPRT transformation, and transformants were confirmed electrophoretically. Measures were taken to ensure that the transformation frequencies observed could not be due to somatic contamination. The positive HPRT transformation result indicates that mature sperm X chromosomal DNA is not modified in the same manner as that of female inactive X chromosomal DNA. Since there is evidence for methylation of the somatic inactive X chromosome, it is possible that methylation, at least for the genes studied, is not involved in sperm X chromosome inactivation.     

Reversal of X-inactivation in female mouse somatic cells hybridized with murine teratocarcinoma stem cells in vitro

A series of near-diploid embryonal carcinoma-like hybrid cells were obtained from polyethylene glycol mediated cell fusion between murine embryonal carcinoma cells (PSA-6TG1 or OTF9-63) having one X chromosome and thymocytes or bone marrow cells from female mice carrying Cattanach's or Searle's translocation. Prior to fusion with EC cells the somatic cells are presumed to contain only one active X chromosome. Following hybrid formation, the chronology of X chromosome replication and the expression of X-linked gene Pgk-1 indicated that all X chromosomes contributed by both parents were active in these hybrids. Experiments were performed to rule out the possibility that the hybrids were formed by fusion of EC cells with rare somatic cells in which both X chromosomes were active. Taken together the data indicate that within four days of fusion there is reactivation of the entire inactive X chromosome.     

Trimethylation of Histone H3 Lysine 4 is an Epigenetic Mark at Regions Escaping Mammalian X Inactivation

It is now estimated that 150-200 genes clustered in several discrete regions escape X inactivation in somatic cells of human females by unknown mechanisms. Here, we show that although the human female inactive X chromosome is largely devoid of histone 3 lysine 4 trimethylation (H3K4me3), regions that are known to escape X inactivation, including the pseudoautosomal regions, are enriched with this modification. Also, H3K4me3, unlike H3K4me2 and H4 and H3 acetylation, is restricted to discrete regions on metaphase chromosomes. In contrast to humans, there are only a few genes that are known to escape X inactivation in the mouse. Therefore, we examined mouse female somatic cells with H3K4me3 to identify candidate regions with genes that escape X inactivation. We found the mouse female inactive X in somatic cells and the male inactive X in meiosis to have seven discrete regions that are enriched with H3K4me3. Furthermore, RNA polymerase II is largely excluded from the XY body at male pachytene except for several discrete regions on the X and Y suggesting the presence of regions that also escape sex chromosome inactivation during male meiosis.     

Proposed Mechanism of Inheritance and Expression of the Human Fragile-X Syndrome of Mental Retardation

A mechanism is proposed for the inheritance and expression of the fragile-X-linked syndrome of mental retardation in humans. Two independent events are required for expression of the syndrome: the fragile-X mutation, and X chromosome inactivation in pre-oogonial cells. The fragile-X mutation at site Xq27 has little or no effect until the chromosome is inactivated in a female as part of the process of dosage compensation. At a stage where the inactivated X chromosome would normally be reactivated in preparation for oogenesis, the mutation results in a local block to the reactivation process. This block to reactivation leads to mental retardation in progeny by reducing the level of products from the unreactivated Xq27 region in male cells, and, for a heterozygous female, in somatic cells in which the normal X chromosome has been inactivated. Published data relevant to this proposed mechanism are discussed.     

Sex chromosome inactivation in the male

Mammalian females have two X chromosomes, while males have only one X plus a Y chromosome. In order to balance X-linked gene dosage between the sexes, one X chromosome undergoes inactivation during development of female embryos. This process has been termed X-chromosome inactivation (XCI). Inactivation of the single X chromosome also occurs in the male, but is transient and is confined to the late stages of first meiotic prophase during spermatogenesis. This phenomenon has been termed meiotic sex chromosome inactivation (MSCI). A substantial portion (~15-25%) of X-linked mRNA-encoding genes escapes XCI in female somatic cells. While no mRNA genes are known to escape MSCI in males, ~80% of X-linked miRNA genes have been shown to escape this process. Recent results have led to the proposal that the RNA interference mechanism may be involved in regulating XCI in female cells. We suggest that some MSCI-escaping miRNAs may play a similar role in regulating MSCI in male germ cells.     

Sex chromosome elimination,X chromosome inactivation and reactivation in the southern brown bandicoot Isoodon obesulus (Marsupialia: Peramelidae)

Cytogenetic studies have shown that bandicoots (family Peramelidae) eliminate one X chromosome in females and the Y chromosome in males from some somatic tissues at different stages during development. The discovery of a polymorphism for X-linked phosphoglycerate kinase (PGK-1) in a population of Isoodon obesulus from Mount Gambier, South Australia, has allowed us to answer a number of long standing questions relating to the parental source of the eliminated X chromosome, X chromosome inactivation and reactivation in somatic and germ cells of female bandicoots. We have found no evidence of paternal PGK-1 allele expression in a wide range of somatic tissues and cell types from known female heterozygotes. We conclude that paternal X chromosome inactivation occurs in bandicoots as in other marsupial groups and that it is the paternally derived X chromosome that is eliminated from some cell types of females. The absence of PGK-1 paternal activity in somatic cells allowed us to examine the state of X chromosome activity in germ cells. Electrophoresis of germ cells from different aged pouch young heterozygotes showed only maternal allele expression in oogonia whereas an additional paternally derived band was observed in pre-dictyate oocytes. We conclude that reactivation of the inactive X chromosome occurs around the onset of meiosis in female bandicoots. As in other mammals, late replication is a common feature of the Y chromosome in male and the inactive X chromosome in female bandicoots. The basis of sex chromosome loss is still not known; however later timing of DNA synthesis is involved. Our finding that the paternally derived X chromosome is eliminated in females suggests that late DNA replication may provide the imprint for paternal X inactivation and the elimination of sex chromosomes in bandicoots.     

Expression of the fragile (X) chromosome in an interspecific somatic cell hybrid

Interspecific somatic cell hybrids were constructed between a Chinese hamster lung cell line deficient in hypoxanthine phosphoribosyltransferase and two lymphoblastoid cultures (GM 4025 and GM 3200) from unrelated males affected with the fragile (X) syndrome. Thirteen independent colonies survived selection in hypoxanthine-azaserine, while only one colony survived selection in hypoxanthine-aminopterin-thymidine. One hybrid formed from GM 4025 was found to contain a human X chromosome as the only detectable human chromosome in the majority of cells analyzed. Induction of fragile (X) expression in this hybrid at frequencies up to 20% was achieved by treatments with 5-fluoro-2'-deoxyuridine (5 X 10(-8) M or 1 X 10(-7) M) or methotrexate (5 X 10(-6) or 1 X 10(-5) for 12 h. Use of the somatic cell hybrid system may allow study of the fragile (X) from different patients on a homogeneous xenogeneic background and may provide a better system for characterization of the fragile (X) at the biochemical and molecular level.