Molecular genetics of cell death in the nematode Caenorhabditis elegans

In C. elegans, cell death can be readily studied at the cellular, genetic, and molecular levels. Two types of death have been characterized in this nematode: (1) programmed cell death, which occurs as a normal component in development; and (2) pathological cell death which occurs aberrantly as a consequence of mutation. Analysis of mutations that disrupt programmed cell death in various ways has defined a genetic pathway for programmed cell death which includes genes that perform such functions as the determination of which cells die, the execution of cell death, the engulfment of cell corpses, and the digestion of DNA from dead cells. Molecular analysis is providing insightinto the nature of the molecules that function in these aspects of programmed cell death. Characterization of some genes that mutate to induce abnormal cell death has defined a novel gene family called degenerins that encode putative membrane proteins. Dominant alleles of at least two degenerin genes, mec-4 and deg-1, can cause cellular swelling and late onset neurodegeneration of specific groups of cells. © 1992 John Wiley & Sons, Inc.     

Primers for the amplification of sequence‐characterized loci in Cryphonectria cubensis populations

We describe the development of DNA markers for the fungal pathogen of Eucalyptus, Cryphonectria cubensis. These markers originated from cloned intershort sequence repeat polymerase chain reactions, which enrich for medium to highly repetitive DNA sequences. In total, 10 markers were isolated, eight of which were polymorphic, and these can subsequently be applied to study populations of C. cubensis.     

Systemic amyloidosis in transgenic mice carrying the human mutant transthyretin (Met 30) gene

To analyze the pathologic processes of amyloid deposition in type I familial amyloidotic polyneuropathy (FAP), mice were made transgenic by introducing the human mutant transthyretin (TTR) gene(MT-hMet 30). An inbred strain of mouse, C57 BL/6, was chosen. Transgenic mice were killed using ether anesthesia at 3-mo intervals up to 24 mo after birth. In these transgenic mice, amyloid deposition started in the gastrointestinal tract, cardiovascular system, and kidneys and extended to various other organs and tissues with advancing age. The pattern of amyloid deposition was similar to that observed in human autopsy cases of FAP, except for its absence in the choroid plexus and in the peripheral and autonomic nervous systems. We extracted the amyloid fibrils from kidneys of these mice with a human mutant TTR gene and analyzed them immunochemically and electronmicroscopically. Deposited amyloid was shown to be composed of human mutant TTR and mouse serum amyloid P component. Amyloid fibril from transgenic mice was morphologically and immunohistochemically similar to that of human FAP. The most striking pathologic feature of the transgenic mice was the absence of amyloid deposition in the peripheral and autonomic nervous tissues. Thus, other intrinsic factors may be involved in amyloid deposition in the nervous tissues of human FAP.     

谷子显性雄性不育基因“Ms~（ch）”的细胞质转换

通过种间杂交和连续置换回交,选育出具有轮生狗尾草（Ｓ,ｖｅｒｔｉｃｉｌｌａｔａ（Ｌ．）Ｂｅａｕｖ．）细胞质的谷子（Ｓｅｔａｒｉａｉｔａｌｉｃａ（Ｌ．）Ｂｅａｕｖ．）核质杂种,以带有上位基因Ｒｆ的显性核不育植株为父本与此核质杂种杂交,已将显性核不育基因导入轮生狗尾草细胞质中,从其分离后代中选出了具有显性核不育基因的新核质杂种,为谷子的三系选育和细胞质研究创造了新工具,也为核互作杂优利用增加了核质互作优势新机制。     

白化病的遗传流行病学研究

本文应用分离分析和血缘分析方法,对山东省１００余万人群遗传病调查中发现的３７个白化病核心家系进行了分析。结果表明：白化病存在遗传异质性,为多基因常染色体隐性遗传,最小基因数为８,平均基因频率为０．００２３,群体中致病基因携带者频率为０．０３８３;近亲结婚大大提高白化病的患病率。     

Dominant rotifers of Võrtsjärv (Estonia)

Rotifers form 71% of the zooplankton of the strongly eutrophic (total N 2 g m^–3, total P 53 mg m^–3) Võrtsjärv (Estonia). Altogether 150 taxa of rotifers occur. Species characteristic of oligo- and mesotrophic waters have totally disappeared during the last 30 years, or are disappearing now. Species whose numbers and biomass reached 20% or more of total zooplankton were considered dominants. These were Anuraeopsis fissa, Keratella cochlearis, K. quadrata frenzeli, Polyarthra dolichoptera, P. luminosa, Synchaeta verrucosa and Trichocerca rousseleti. The contribution of dominant rotifers to total zooplankton and its biomass is as follows: S. verrucosa 25% and 39%, P.dolichoptera 34% and 25%, K. cochlearis 25% and 7%, K. quadrata frenzeli 9% and 7%, A. fissa 28% and 0.4%, T. rousseleti 20% and 0.6%, respectively.     

X-linked dominant inheritance of partial phosphorylase kinase deficiency in mice

A new mouse strain, the V strain, with a partial deficiency of phosphorylase kinase has been established. The deficiency is caused by an X-linked dominant gene (Phk ^c ). Muscle extracts of homozygous and heterozygous females and hemizygous males have about 25% of the activity found in extracts of normal (C3H/HeHan) mice. This dominant phosphorylase kinase deficiency of the new V strain is different from that of the I-strain mice with the X-linked recessive deficiency of skeletal muscle phosphorylase kinase. The muscle extracts of V-strain and normal mice contain the same phosphorylase phosphatase activity of about 1 U/mg. Heart and liver extracts from V mice contained about 50% and 66%, respectively, of the phosphorylase kinase activity compared to that found in the same organs from the normal mice. The glycogen content of the skeletal muscle of the V strain was normal, i.e., 0.9 mg/g. Phosphorylase kinase was purified from the skeletal muscle of the V strain by (a) hydrophobic chromatography on methylamine Sepharose, (b) ammonium sulfate precipitation, and (c) gel filtration of Sepharose 4B. The enzyme has a similar structure to the normal murine and rabbit skeletal muscle enzyme, except that the proportion of the subunits differs. The molar ratio of the subunits of the V strain mice is (+)::=0.54:1:1.169, in comparison with that of the rabbit (+)::=1.1:1.0:1.0 and that of normal murine enzyme 0.9:1.0:0.7.This work was supported by the Minister für Wissenschaft und Forschung des Landes Nordrhein-Westfalen, West Germany and of the Fonds der Chemie, West Germany, and forms part of the md thesis of A. Vrbica.     

阿尔泰山萨彦岭4种优势树种径向生长对气候因子的响应

气候变化深刻地影响森林树木的生长,而树种对气候变化敏感度的差异可能影响了气候变化下的森林生态系统响应。因此,研究优势树种间生长对气候变化的敏感度差异,对正确认识气候变化下林分生长动态及分布格局十分重要。基于树木年代学的方法,研究了阿尔泰山萨彦岭西伯利亚落叶松（Larix sibirica）、西伯利亚红松（Pinus sibirica）、西伯利亚冷杉（Abies sibirica）以及西伯利亚云杉（Picea obovata）4种优势树种的径向生长-气候关系。结果显示：（1）西伯利亚冷杉径向生长与上一年10-11月、当年1-9月的干旱指数、2-4月的降水显著正相关,与1月的平均温和最高温呈显著负相关关系,与当年4、6月份的水汽压正相关;（2）西伯利亚落叶松径向生长与上一年8月和当年8月的平均温、最高温以及当年8月的最低温显著负相关,而与当年6月的最低温则正相关,与8月份的水汽压显著负相关;（3）西伯利亚红松径向生长与3月降水、7月最低温、上一年10月的水汽压显著正相关;（4）西伯利亚云杉径向生长与6月平均温、最高温、水汽压正相关,与上一年10-11月、当年2-4月和9月的干旱指数正相关,同时与3、4月的降水量显著正相关。西伯利亚冷杉和西伯利亚云杉、西伯利亚云杉和西伯利亚落叶松、西伯利亚云杉和西伯利亚红松对于特定气候因子表现出相似的响应结果,与年表间相关性的结果一致。但差异也是明显的,西伯利亚冷杉和西伯利亚云杉对区域水分变化敏感,而西伯利亚落叶松和西伯利亚红松主要对区域温度变化敏感。综上所述,气候变化下,该区域优势树种对气候变化响应的差异可能导致区域林分动态和格局的改变,因此,多树种径向生长-气候关系研究有助于正确反映森林动态。研究结果可以为区域森林管理与生态保护工作提供理论依据。