黑腹果蝇P转座因子研究 Ⅰ.我国黑腹果蝇的P-M测定及其地理分布

采用性腺败育(GD不育)作为标准检定方法。对我国20个地方的黑腹果蝇的P因子活性和细胞型进行了测定。结果表明我国北部沿海城市为Q型;南部沿海和内地皆为M型。各地的M品系所产生的GD不育能力各不相同,但表现出与地理位置相关的梯度变化。这一变化规律为研究我国黑腹果蝇的P因子起源及P和M品系的形成提供了重要的理论依据。     

Apolipoprotein A-I metabolism in subjects with a PstI restriction fragment length polymorphism of the apoA-I gene and familial hypoalphalipoproteinemia

Familial hypoalphalipoproteinemia (hypoalpha), characterized by a decreased high density lipoprotein level, is associated with an increased incidence of premature cardiovascular disease. Restriction fragment length polymorphism analysis of genomic DNA has detected a polymorphism for the PstI restriction endonuclease near the apoA-I gene, with either a 2.2 or a 3.3 kb fragment. The latter has been previously found to occur with significantly higher frequency in probands of families with familial hypoalpha. ApoA-I was isolated from three unrelated subjects with familial hypoalpha and the 3.3 kb PstI polymorphism of the apoA-I gene, and from normal control subjects. The apoA-I from the hypoalpha subjects was structurally normal as determined by amino acid analysis and by two-dimensional gel electrophoresis. When normal apoA-I and hypoalpha apoA-I were simultaneously injected into either normal controls or hypoalpha subjects, both forms of apoA-I were catabolized at the same rate in the same subject, indicating that the hypoalpha apoA-I is also metabolically normal. Analysis of the kinetics of metabolism of apoA-I in the hypoalpha subjects, compared to the normal controls, revealed that the reduced plasma levels of apoA-I were due to an increased apoA-I fractional catabolic rate, and that the synthetic rate was normal. Based on these results, we conclude that the apoA-I gene in these hypoalpha subjects is normal, and the PstI polymorphism near the apoA-I gene, which is associated with familial hypoalpha, is likely to be a marker for a mutant gene closely linked to, but not in, the apoA-I gene.     

小鼠LAK细胞对红系祖细胞及多向造血祖细胞增殖的影响

小鼠脾细胞经重组人白细胞介素-2(rhIL-2)激活后对YAC-1,LP-3和WEHI-164等肿瘤细胞均有很强的杀伤活性。在CFU-E和BFU-E培养体系中,不同浓度LAK细胞与BMC直接加入或预温育4h后再培养,均能加强CFU-E和BFU-E增殖。低浓度LAK细胞(LAK/BMC为0.5)与BMC直接加入或预温育后再加入CFU-mix培养体系中,均能增强CFU-mix增殖,而高浓度LAK细胞和BMC(LAK/BMC=8.0)直接加入培养体系则抑制CFU-mix增殖;若共温育后再培养则非常明显地抑制CFU-mix增殖,CFU-mix仅为对照的17.6％。小鼠LAK细胞对造血祖细胞体外增殖具有调节作用,这种调节可能包括分泌某些细胞因子以及细胞间直接相互作用两种方式。     

肿瘤抑制基因APCmRNA在豚鼠脑中的分布

APC基因是1991年被发现的一类肿瘤抑制基因,它被定位于人第5号染色体5q21处。APC基因如发生缺失或突变,则易患直肠肿瘤,并伴有部分先天痴呆的病例。本工作在孟帆已获得的APC基因在豚鼠中的同源cDNA的基础上,完成了对它的亚克隆,并利用原位杂交和RNA酶保护分析的方法,对它在脑中的分布进行了研究。发现APCmRNA主要在海马、大脑和小脑中表达;嗅球中杂交信号稍弱,脑干中最弱。海马中阳性细胞主要是锥体细胞,小脑中则主要是内层颗粒细胞。在一个月大的豚鼠胚胎的脑中也观察到相似的表达型式。进一步的研究有助于我们更好地了解神经发育和先天痴呆发生的分子机制。     

原噬菌体PBSX阻遏基因及其温度敏感型等位基因的克隆分析

本研究利用聚合酶链式反应技术,成功地克隆了枯草芽孢杆菌缺陷型原噬菌体ＰＢＳＸ阻遏基因及其温度敏感型等位基因。核苷酸序列分析发现,野生型及其温度敏感型阻遏基因之间的碱基变异较大,但却存在几乎完全相同的开放读框,尤其是开放读框ｏｒｆⅠ,可能编码着１１３个氨基酸的阻遏蛋白,并且还推定了开放读框的启动区和核糖体结合位点。通过互补实验,证实了野生型阻遏基因的产物能够抑制温度诱导ＰＢＳＸ原噬菌体,表明克隆的基因有着正常的生物活性。