Bemerkungen zur Variabilität vonSaxifraga marginata

Saxifraga marginata Sternb. is divided into three subspecies:S. m. subsp.marginata, S. m. subsp.bubakii (Rohlena)Chrtek etSoják,S. m. subsp.karadzicensis (Degen etKo?anin)Chrtek etSoják (environments of Skopje, Macedonia).     

正丁酸钠对人胃腺癌细胞染色体数目和DNA含量的影响

培养的人胃腺癌MGc 80-3细胞经过正丁酸钠处理7天后,生长抑制率达50.7%,约有90%的细胞形态发生分化,其超微结构亦有显著改变。而且,在染色体数目上,超二倍体细胞由对照组的78%增加到实验组的96%,超三倍体和超四倍体细胞则分别从6%和14%下降至2%。同时应用~3H-TdR放射自显影和福尔根细胞光度法测定未标记细胞(G_1期)DNA含量,结果显示实验组比对照组降低了。而且在实验组的同一制片中,未分化细胞DNA含量平均为超六倍体值(DI=3.67和3.56),其中90%的细胞超过6C;分化细胞DNA含量则平均为近四倍体值(DI=2.03和1.99),其中近60%的细胞少于4C。两者差异统计显著,表明形态分化的人胃腺癌细胞的遗传物质含量明显减少,但这些细胞并非就是正常二倍体细胞。     

云南10个民族红细胞酸性磷酸酶型分布调查

用淀粉凝胶电泳法对云南省汉族及9个少数民族的红细胞酸性磷酸酶(ACP_1)的表型分布进行了调查,检出A、BA和B3种表型,计算得云南汉、彝、白、傣、瑶、佤、哈尼、布朗、基诺和拉祜族ACP_1~A、ACP_1~B的基因频率依次为0.2067、0.7933;0.2406、0.7594;0.2341、0.7659;0.3750、0.6250;0.2300、0.7700;0.2727、0.7273;0.3594、0.6406;0.3036、0.6964;0.2381、0.76119和0.4474、0.5526。未发现ACP_1~C基因及其它稀有基因。研究表明,ACP_1表型的分布存在着一定的种族与民族差异。     

甘蔗幼叶切段培养中的体细胞胚胎发生

本文从形态学和组织学方面研究了甘蔗幼叶胚性愈伤组织发生及体细胞胚胎的形成过程。甘蔗幼叶片切段培养于含2.4—D1.5mg/1的MS培养基上,4—6天后切段开始形成愈伤组织,约10天后愈伤组织表面出现白色颗粒状结构。将含有白色颗粒状结构的愈伤组织转移至不含激素的培养基中,7—10天后可见有小植株长出。组织学和形态学观察表明,甘蔗离体再生植株是通过体细胞胚胎发生途径。     

Characterization of Senescence in Lemna gibba G3: A Determinate Growth System

Frond senescence in Lemna gibba G3 was characterized, and itscontrol by light, ABA and kinetin investigated. The plant exhibitsa determinate growth pattern with a frond producing a set numberof daughter fronds before undergoing senescence and death regardlessof whether or not it flowers. When a frond was cut in half,the distal half (half frond) which lacks any meristem underwentrapid senescence as compared with intact fronds. In both intactand half fronds, the onset of senescence was accelerated byABA and retarded by kinetin. Continuous white light acceleratedsenescence in both intact and half fronds over the dark controls.Under different photoperiodic light regime, the pace of daughterfrond production is accelerated in proportion to the lengthof light period. In half fronds, however, very short photoperiodiclight treatments (e.g. 1L: 23D or 3L: 21D) rather delayed senescenceover the dark controls. Two separate light control systems operatingin opposite directions in Lemana senescence appear to exist. ¹Present address: Department of Biology, Yonsei University,Seoul 120-749, Korea ²Present address: U.S. Department of Agriculture, Aero SpaceBuilding, Rm. 323, 901 D Street, S.W., Washington, D.C. 20251-2200, U.S.A. (Received July 13, 1989; Accepted May 8, 1990)     

棕色固氮菌缺失nifZ基因的突变种固氮酶MoFe蛋白的纯化和性质

采用 52℃下加热 6 min,后经 DEAE- 52、Sephacryls S- 2 0 0和 Q- Sepharose等柱层析方法 ,分离纯化了棕色固氮菌 (Azotobacter vinelandii)缺失 nif Z基因突变种固氮酶 Mo Fe(Δnif Z Mo Fe)蛋白 ,其纯度达到电泳纯。Δnif Z Mo Fe蛋白的固氮活性为 2 83nmol C2 H2 还原 / (min·mg蛋白 ) ,远低于野生种 Mo Fe蛋白。Δnif Z Mo Fe蛋白对氧更敏感 ;热稳定性略低于野生种。Δnif Z Mo Fe蛋白的可见光吸收光谱与野生种 Mo Fe蛋白极为相似。其圆二色谱和磁圆二色谱在 450～ 550 nm与野生种 Mo Fe蛋白显著不同 ,表明其 P- cluster及其周围环境与野生种 Mo Fe蛋白有所差异。这亦可能是造成缺失 nif Z突变种 Mo Fe蛋白固氮活性低的原因。     

Interactions between the ankyrin repeat-containing protein Akr1p and the pheromone response pathway in Saccharomyces cerevisiae.

Akr1p, which contains six ankyrin repeats, was identified during a screen for mutations that displayed synthetic lethality with a mutant allele of the bud emergence gene BEM1. Cells from which AKR1 had been deleted were alive but misshapen at 30 degrees C and inviable at 37 degrees C. During a screen for mutants that required one or more copies of wild-type AKR1 for survival at 30 degrees C, we isolated mutations in GPA1, which encodes the G alpha subunit of the pheromone receptor-coupled G protein. (The active subunit of this G protein is G beta gamma, and G alpha plays an inhibitory role in G beta gamma-mediated signal transduction.) AKR1 could serve as a multicopy suppressor of the lethality caused by either loss of GPA1 or overexpression of STE4, which encodes the G beta subunit of this G protein, suggesting that pheromone signaling is inhibited by overexpression of Akr1p. Mutations in AKR1 displayed synthetic lethality with a weak allele of GPA1 and led to increased expression of the pheromone-inducible gene FUS1, suggesting that Akr1p normally (and not just when overexpressed) inhibits signaling. In contrast, deletion of BEM1 resulted in decreased expression of FUS1, suggesting that Bem1p normally facilitates pheromone signaling. During a screen for proteins that displayed two-hybrid interactions with Akr1p, we identified Ste4p, raising the possibility that an interaction between Akr1p and Ste4p contributes to proper regulation of the pheromone response pathway.