Acyl-CoA oxidase from Candida tropicalis

Acyl coenzyme A oxidase (acyl-CoA oxidase) has been isolated in good yield from Candida tropicalis pK 233 grown on n-alkanes. Gel filtration, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and measurement of flavin content suggest that the oxidase is an octamer of Mr 75 000 subunits each containing one flavin. The oxidase yields the red semiquinone form on dithionite or photochemical reduction, slowly forms an N-5 adduct with 0.16 M sulfite at pH 7.4, and is rapidly reduced by borohydride, forming the 3,4-dihydroflavin isomer. The red flavosemiquinone is only kinetically stabilized with respect to disproportionation in the free enzyme but is thermodynamically stabilized on binding enoyl-CoA derivatives. The enzyme is reduced by butyryl-, octanoyl-, and palmitoyl-CoA without formation of prominent long-wavelength bands. Acyl-CoA oxidase and the acyl-CoA dehydrogenases share many similarities in their interaction with CoA derivatives. For example, both enzymes stabilize the anionic radical on binding enoyl-CoA derivatives, both dehydrogenate 2-oxoheptadecyldethio-CoA but cannot utilize S-heptadecyl-CoA, both form long-wavelength bands with CoA persulfide species, and both enzymes are attacked by the suicide substrates 3,4-pentadienoyl-CoA and (methylene-cyclopropyl)acetyl-CoA at the flavin prosthetic group.     

广西贵县的螟害规律及其预测方法的探讨

1.从广西贵县1958—1964年的七年螟害调查资料,可以将全年螟害的消长趋势,划分为世代递减发生型、世代递增发生型和第三世代多发型等三种螟害发生型。 2.形成三种螟害发生型的原因,主要系由于水稻播植期的早晚与螟虫发生为害的不同组合所致。水稻播植期较早的年份,形成世代递减发生型;播植期较晚的年份,形成世代递增发生型:播植期居中的年份,则形成第三世代多发型。 3.本文根据历史资料,订出早、中、晚播植期的标准,以此标准为坐标图上的横轴,各世代螟害率为纵轴,作出了播种期与螟害型的关系模式图。根据这个模式图,在某年掌握了早稻播种期以后,就可以作出该年螟害发生发展趋势的展望。 4.求算三种螟害发生型各世代之间的螟害增减比值历年平均数,在某年获悉早稻播种期和第一世代实测螟害率以后,就可以根据这个比值平均数,依次推算以后各世代的预测螟害率。 5.关于各世代螟害率的近期预测,本文主张以幼虫虫口密度为依据,求算虫口密度与其所造成螟害率的二次函数曲线方程式,在获得幼虫密度以后,代入方程式来计算近期预测的螟害率。     

溴氰菊酯对鼠脑蛋白质磷酸化作用的影响

以小鼠大脑碎片与[γ-~(32)P]ATP一起保温,观察到溴氰菊酯对蛋白1—3磷酸化的刺激作用和对4、5磷酸化的抑制作用,表明溴氰菊酯对大脑蛋白质磷酸化产生了影响。从鼠脑分离了C、D、S三个组分,分别进行的蛋白质磷酸化试验结果表明,C、D组分可能是重要的磷酸化部位。 蛋白1、2、3的磷酸化明显地受到溴氰菊酯的刺激,这三个蛋白质可能是“蛋白Ⅲb”的几种形式。溴氰菊酯对“蛋白Ⅲb”磷酸化的刺激,可能会影响神经末梢的神经激素释放,从而影响到与其相关的某些神经功能。     

生物素标记寡核苷酸探针探测扩增的病理性突变珠蛋白基因

用末端转移酶催化生物素核苷酸底物(Biotin-ll-dUTP)共价连接在合成的寡核苷酸3’羟基末端,从而合成了两种寡核苷酸探针(β~T_(41-42)及β~A_(41-42))。用它们分别与克隆化扩增的正常和突变的β—珠蛋白基因片段杂变。结果表明该探针都具有与~(32)P探针相似的特异性,其杂交的灵敏度为2—3pg(特异序列)。进而将探测HbS基因的正常和异常两种寡核苷酸19聚体(β~A_6和β~S_6)用~(32)P和生物素分别标记;将HbS杂合子病人的白细胞DNA经聚合酶链反应(PCR)法扩增,并以含正常β—珠蛋白基因的DNA片段作对照,与两种探针分别进行斑点杂交。所得结果完全一致;Hbs杂合子DNA对正常和异常探针都显出杂交信号,而正常DNA只与β~A探针显杂交信号。     

镉引起小麦苗逆境乙烯的产生及其和镉的吸收分布的关系

溶液培养小麦幼苗转移至含Cd~(2 )的营养液中,根系乙烯产生较快地增加,约在12h达高峰,然后下降;ACC含量亦呈先升后降的趋势。未和Cd~(2 )溶液直接接触的地上部乙烯亦增加,至36h达高峰,此后急剧下降,而ACG和 MAGC含量持续上升。地上部乙烯的增加,主要是由通过根系运往地上部的镉直接作用的结果,不是根部合成ACG运往地上部后再产生的。电镜观察表明,地上部乙烯产生和ACC含量变化的时间进程,可以与镉进入叶细胞内的部位及其对细胞膜和细胞器的影响相联系。     

棉属栽培种与野生种杂交的不亲和性

本文研究了棉属栽培种与野生种杂交的不亲和性,试验材料涉及5个染色体组,包括2个栽培种(陆地棉和中棉)和5个野生种(戴维逊氏棉、瑟伯氏棉、三裂棉、阿拉伯棉和比克氏棉)。以陆地棉作母本,异己花粉管在花柱中生长缓慢,有花粉管胚珠低于10%,陆地棉×戴维逊氏棉杂种胚在子叶期坏死。以中棉作母本,不亲和性主要表现在受精后的胚胎发育过程中。     

城市中的伴人植物

伴人植物分布于城市中的许多地方,常被视为杂草而清除。本文论述了城市伴人植物的特点、分布,及其在城市环境保护及美化中的作用,最后列出了北方城市中一些常见伴人植物的名称。     

Nucleocytoplasmic transport is enhanced concomitant with nuclear accumulation of epidermal growth factor (EGF) binding activity in both 3T3-1 and EGF receptor reconstituted NR-6 fibroblasts

Measurements of nucleocytoplasmic transport of fluorescent-labeled macromolecules were performed in both an EGF-nonresponsive mutant fibroblast line (3T3-NR6) and in the same cell line reconstituted with active EGF receptors derived from rat hepatic membrane fraction. Immunolocalization studies of exogenously incorporated EGF receptors in reconstituted 3T3-NR6 fibroblasts demonstrated predominantly intracellular localization. The EGF receptor constructs also showed EGF-stimulated incorporation of [3H]thymidine, providing biochemical evidence for functional integration of the exogenously supplied EGF receptors into the reconstituted fibroblasts. Additional support for the functional incorporation of receptor may be inferred from the enhanced cellular accumulation of 125I-EGF in cells treated with chloroquine and leupeptin. 125I-EGF binding and transnuclear macromolecular transport measurements in mutant and reconstituted cells, in conjunction with such measurements on nuclei isolated from these cells, provide data consistent with a growth factor/nuclear signaling mechanism dependent on the nuclear acquisition of EGF binding activity from the plasma membrane.     

Purification of the 110-kilodalton glycoprotein receptor for mouse hepatitis virus (MHV)-A59 from mouse liver and identification of a nonfunctional, homologous protein in MHV-resistant SJL/J mice.

The receptor for mouse hepatitis virus strain A59 (MHV-A59) is a 110- to 120-kilodalton (kDa) glycoprotein which is expressed in MHV-susceptible mouse strains on the membranes of hepatocytes, intestinal epithelial cells, and macrophages. SJL/J mice, which are highly resistant to MHV-A59, were previously shown to lack detectable levels of receptor by using either solid-phase virus receptor assays or binding of a monoclonal anti-receptor antibody (MAb) which blocks infection of MHV-susceptible mouse cells. This MAb was used for affinity purification of the receptor glycoprotein from livers of MHV-susceptible Swiss Webster mice. The MHV receptor and an antigenically related protein of 48 to 58 kDa were copurified and then separated by preparative sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The first 15 amino acids of the receptor were sequenced, and a synthetic peptide of this amino acid sequence was prepared. Rabbit antiserum made against this peptide bound to the MHV receptor glycoprotein and the 48- to 58-kDa protein from livers of MHV-susceptible BALB/c mice and Swiss Webster mice and from the intestinal brush border of BALB/c mice. In immunoblots of intestinal brush border and hepatocyte membranes of MHV-resistant SJL/J mice, the antibody against the amino terminus of the receptor identified proteins that are 5 to 10 kDa smaller than the MHV receptor and the 48- to 58-kDa related protein from Swiss Webster or BALB/c mice. Thus, SJL/J mice express a protein which shares some sequence homology with the MHV receptor but which lacks virus-binding activity and is not recognized by the blocking anti-receptor MAb. These results suggest that resistance of SJL/J mice to MHV-A59 may be due to absence or mutation of the virus-binding domain in the nonfunctional receptor homolog in SJL/J mice.