A revision of the genus Annesorhiza (Apiaceae)

The genus Annesorhiza is revised and twelve species are recognized, of which two are newly described: A. altiscapa, A. burttii, A. flbrosa, A. flagellifolia, A. grandiflora, A. lateriflora, A. latifolia, A. macrocarpa, A. nuda, A. schlechteri, A. thunbergii and A. wilmsii. A. marlothii is reduced to synonymy under A. lateriflora , a species hitherto poorly known as Peucedanum lateriflorum. A. thunbergii is only known from the type specimen. A. elata, A. hirsuta and A. villosa are sunk under A. grandiflora. A. fúicaulis has recently been excluded from Annesorhiza on the basis of fruit structure. A key to the species is provided, an update on the nomenclature, typification of names and distribution maps are provided for all the species.     

Three new species of Aiphanes (Palmae) with notes on the genus in Ecuador

Twelve species of the palm genus Aiphanes occur in Ecuador. The morphological variation in the genus is surveyed, and the distribution of the Ecuadorean species is discussed. A key to the species of Aiphanes in Ecuador is provided. Aiphanes chiribogensis, A. grandis , and A. verrucosa are described as new species, and illustrated. Aiphanes caryotifolia, A. eggersii, A. erinacea, A. fosteriorum, A. gela-tinosa, A. macroloba, A. schultzeana , and A. tricuspidata are characterized. One still unidentified species resembling A. tessmannii is discussed.     

Systematic studies on the Pompilidae occurring in Japan: Genus Agenioideus Ashmead (Hymenoptera), supplement

Two species of the pompilid genus Agenioideus occurring in Japan are described: A . ( Agenioideus ) kokyo and A . ( A .) cinctellus . The former is new to science and the latter is recorded from Japan and Taiwan for the first time. A brief summary of the biology of A. cinctellus , distinguishing characters between A. ( A. ) ishikawai Shimizu, 1989 and its relatives, and a key to all Japanese species of this genus are presented. Psammochares cinctellus f. rufa Haupt, 1938 and A . ( A. ) pacificus Lelej, 1994 are newly synonymized with A. cinctellus . A new combination is proposed: A . ( A .) maculipes (Smith, 1870) (= Pompilus maculipes Smith), which is found in Southeast Asia to South Asia. Agenioideus ishikawai is newly recorded from Korea and China.     

The glio-toxic mechanism of α-aminoadipic acid on cultured astrocytes

The mechanism of action of the glutamate analogue α-aminoadipic (A A A) acid was investigated in terms of its toxicity to cultured astrocytes. A A A was more toxic to type 1 astrocytes than type 2 astrocytes. Also the higher toxicity of the L-isomer as compared to the D-isomer was seen on type 1 astrocytes but not type 2. The toxicity of A A A can be reduced by co-culture of type 1 astrocytes with microglia. This inhibition may be due to glutamate release by microglia. No such effect is seen for type 2 astrocytes. The major uptake route for A A A by type 1 astrocytes is through the sodium dependent glutamate port. Both isomers of A A A are toxic to dividing astrocytes. The D-isomer appears to be toxic only for mitotic cells. The mechanism of this toxicity is protein synthesis dependent. It is suggested that A A A is toxic to mitotic astrocytes by interference with protein synthesis needed for cell division. D-A A A as opposed to L-A A A may prove a valuable tool for investigation of astrocyte proliferation in development and disease.     

Isoprenylation is required for the processing of the lamin A precursor

The nuclear lamina proteins, prelamin A, lamin B, and a 70-kD lamina-associated protein, are posttranslationally modified by a metabolite derived from mevalonate. This modification can be inhibited by treatment with (3-R,S)-3-fluoromevalonate, demonstrating that it is isoprenoid in nature. We have examined the association between isoprenoid metabolism and processing of the lamin A precursor in human and hamster cells. Inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase by mevinolin (lovastatin) specifically depletes endogenous isoprenoid pools and inhibits the conversion of prelamin A to lamin A. Prelamin A processing is also blocked by mevalonate starvation of Mev-1, a CHO cell line auxotrophic for mevalonate. Moreover, inhibition of prelamin A processing by mevinolin treatment is rapidly reversed by the addition of exogenous mevalonate. Processing of prelamin A is, therefore, dependent on isoprenoid metabolism. Analysis of the conversion of prelamin A to lamin A by two independent methods, immunoprecipitation and two-dimensional nonequilibrium pH gel electrophoresis, demonstrates that a precursor-product relationship exists between prelamin A and lamin A. Analysis of R,S-[5-3H(N)]mevalonate-labeled cells shows that the rate of turnover of the isoprenoid group from prelamin A is comparable to the rate of conversion of prelamin A to lamin A. These results suggest that during the proteolytic maturation of prelamin A, the isoprenylated moiety is lost. A significant difference between prelamin A processing, and that of p21ras and the B-type lamins that undergo isoprenylation-dependent proteolytic maturation, is that the mature form of lamin A is no longer isoprenylated.     

12种中国葱属植物的核型分析

采用细胞压片法,对采自中国西部的12种葱属植物的根尖有丝分裂中期进行了观察,其巾天蓝韭(A.cyaneum)、梭沙韭(Aforrestii)、昌都韭(A.changduense)、西川非(A.xichuanense)、野黄韭(A.rude)、野葱(A.chrysanthum)和真籽韭(A.eusperma)等7种植物的核型为首次报道.供试类群中,峨眉韭(A.omeiense)和多星韭(A.wallichii)的染色体基数分别为11和7,其余类群的染色体基数均为8.观察发现,随体杂合和多侪性现象在供试类群中很普遍.分析推测:(1)随体和倍性的变异在葱属某些类群的进化中可能起重要作用,随体的类型在葱属具有重要的分类意义;(2)多倍化和地下走茎的无性繁殖方式可能是天蓝韭(A.cyaneum)的进化策略;(3)西川韭(A.xichuanense)、野黄非(A.rude)和野葱(A.chrysanthum)有密切的亲缘关系;(4)真籽韭(A.eusperma)与多籽组在核型上有密切的亲缘关系.     

中国东北科尔沁沙地两种建群植物的抗旱机理

在土壤田间持水和干旱胁迫条件下,对冷蒿和差巴嘎蒿的多个抗旱性生理指标进行了测定,结果表明:1、在两种土壤水分状况下,冷蒿的水势低于差巴嘎蒿,水分相对亏缺、束缚水含量、束缚水与自由水比值、综合抗旱性指数均明显高于差巴嘎蒿,且胁迫前后冷蒿上述指标的变化幅度高于差巴嘎蒿。2、土壤田间持水量条件下冷蒿干物质累积量、硝态氮含量和硝酸还原酶活性高于差巴嘎蒿,可溶性蛋白质含量和叶绿素含量低于差巴嘎蒿。水分胁迫发生时,冷蒿蛋白质降解的幅度高于差嘎蒿;冷蒿体内脯氨酸的累积量可达胁迫前的8.2倍,差巴嘎蒿只达原来的2.2倍;冷蒿可溶性糖含量达胁迫前的1.29倍,差巴嘎蒿只达胁迫前的0.37倍;胁迫条件下冷蒿的叶绿素含量高于差巴嘎蒿。3、严酷的沙区环境条件下,冷蒿在一日内各时刻的蒸腾速率和水势均低于差巴嘎蒿,且日间波动平缓。     

Interaction between S100A8/A9 and annexin A6 is involved in the calcium-induced cell surface exposition of S100A8/A9

The calcium binding S100A8/A9 complex (MRP8/14; calgranulin) is considered as an important proinflammatory mediator in acute and chronic inflammation and has recently gained attention as a molecular marker up-regulated in various human cancers. Here, we report that S100A8/A9 is expressed in breast cancer cell lines and is up-regulated by interleukin-1beta and tumor necrosis factor-alpha in SKBR3 and MCF-7 cells. We identified the phospholipid-binding protein annexin A6 as a potential S100A8/A9 binding protein by affinity chromatography. This finding was verified by Southwestern overlay experiments and by coimmunoprecipitation with the S100A8/A9-specific monoclonal antibody 27E10. Immunocytochemical experiments demonstrated that S100A8/A9 and annexin A6 colocalize in SKBR3 breast cancer cells predominantly in membranous structures. Upon calcium influx both S100A8/A9 and annexin A6 are exposed on the cell surface of SKBR3 cells. Subcellular fractionation studies suggested that after A23187 stimulation membrane association of S100A8/A9 is not enhanced. However, both S100A8/A9 and annexin A6 are exposed on the cell surface of SKBR3 cells upon calcium influx. Experiments with artificial liposomes indicated that S100A8/A9 is able to associate with membranes independently of both annexin A6 and independently of calcium. Finally, cell surface expression of S100A8/A9 could not be observed in A23187-treated A431 and HaCaT cells. Both cell lines are known to be devoid of annexin A6. Repression of annexin A6 expression by small interfering RNA in SKBR3 cells abolishes the cell surface exposition of S100A8/A9 upon calcium influx, suggesting that annexin A6 contributes to the calcium-dependent cell surface exposition of the membrane associated-S100A8/A9 complex.     

The Mutation SK(ad-3A) Cancels the Dominance of ad-3A+ over ad-3A in the Ascus of Neurospora

A newly induced mutant of Neurospora, when crossed with an ad-3A mutant, produces asci with four viable black and four inviable white ascospores. The survivors always contain the new mutant allele, never ad-3A. The new allele, which is called SK(ad-3A) (for spore killer of ad-3A), is located at or very near the ad-3A locus.--In crosses homozygous for ad-3A, each ascus contains only inviable white ascospores. This defect in ascospore maturation is complemented by the wild-type allele, ad-3A+ (crosses heterozygous for ad-3A and ad-3A+ produce mainly viable ascospores), but it is not complemented by the new SK(ad-3A) allele (all ad-3A ascospores from crosses heterozygous for SK(ad-3A) and ad-3A are white and inviable). In crosses homozygous for SK(ad-3A) or heterozygous for SK(ad-3A) and ad-3A+, each ascus contains only viable black ascospores. SK(ad-3A) does not require adenine for growth, and forced heterokaryons between SK(ad-3A) and ad-3A grow at wild-type rates and produce conidia of both genotypes with approximately equal frequency. Thus, the action of SK(ad-3A) is apparently restricted to ascospore formation. Possible mechanisms of the action of this new allele are discussed.     

Probing the local conformational change of alpha1-antitrypsin

The native form of serpins (serine protease inhibitors) is a metastable conformation, which converts into a more stable form upon complex formation with a target protease. It has been suggested that movement of helix-F (hF) and the following loop connecting to strand 3 of beta-sheet A (thFs3A) is critical for such conformational change. Despite many speculations inferred from analysis of the serpin structure itself, direct experimental evidence for the mobilization of hF/thFs3A during the inhibition process is lacking. To probe the mechanistic role of hF and thFs3A during protease inhibition, a disulfide bond was engineered in alpha(1)-antitrypsin, which would lock the displacement of thFs3A from beta-sheet A. We measured the inhibitory activity of each disulfide-locked mutant and its heat stability against loop-sheet polymerization. Presence of a disulfide between thFs3A and s5A but not between thFs3A and s3A caused loss of the inhibitory activity, suggesting that displacement of hF/thFs3A from strand 5A but not from strand 3A is required during the inhibition process. While showing little influence on the inhibitory activity, the disulfide between thFs3A and s3A retarded loop-sheet polymerization significantly. This successful protein engineering of alpha(1)-antitrypsin is expected to be of value in clinical applications. Based on our current studies, we propose that the reactive-site loop of a serpin glides through between s5A and thFs3A for the full insertion into beta-sheet A while a substantial portion of the interactions between hF and s3A is kept intact.     

横断山区四种湍蛙的细胞遗传学研究

通过染色体组型分析,C带(BSG技术)分析及一种简便的Ag-NORs带分析,对四川湍蛙、理县湍蛙、棕点湍蛙和棘皮湍蛙的种间关系、染色体的演化及其性染色体等问题进行了初步探讨。结果表明:(1)四川湍蛙、理县湍蛙和棕点湍蛙之间的亲缘关系较近,而它们与棘皮湍蛙的亲缘关系较远;(2)在近缘种的分化中,染色体结构异染色质的变化和臂间倒位是重要的因素之一,这在小型染色体上表现得尤为突出;(三)四川湍蛙具有在形态上分化很明显的性染色体。C带分析表明,此性染色体主要由常染色质构成,但在其Y染色体的长臂上存在明显的中间C带,推测尚处于性染色体分化的初期阶段。     

Analysis of β3-endonexin mutants for their ability to interact with cyclin A

We have recently identified beta(3)-endonexin as a molecule that interacts with cyclin A-associated kinase. In this study, beta(3)-endonexin mutants were constructed by PCR-based site-directed mutagenesis, and characterized. Beta(3)-endonexin has a cyclin binding motif, RxL, in its N-terminal region, and two SP sequences which resemble a known target site for cyclin-dependent kinases (Cdks). The R5A/L7A mutant of beta(3)-endonexin, in which the RxL motif has been changed to AxA, is unable to bind to cyclin A, as revealed by two-hybrid experiments and in vitro pull-down assays. A GST-beta(3)-endonexin fusion, but not the corresponding R5A/L7A mutant, inhibits phosphorylation of Rb protein by cyclin A/Cdk2 in vitro. A cyclin A/Cdk2 kinase complex produced in, and purified from, insect cells phosphorylated GST-beta(3)-endonexin in vitro. The S33A or S46A mutant is partially phosphorylated by cyclin A/Cdk2, whereas no phosphorylation of the S33A/S46A double mutant is detectable. This demonstrates that these two serine residues, each of which is followed by a proline residue, are target sites for phosphorylation by cyclin A-associated kinase. The R5A/L7A mutant form of beta(3)-endonexin, which is defective for binding to cyclin A, is also not phosphorylated by cyclin A/Cdk2, confirming that the phosphorylation requires binding to cyclin A in the kinase complex. The neutralizing effect of beta(3)-endonexin on the toxicity associated with the expression of full-length human cyclin A in budding yeast is correlated with its ability to bind to cyclin A. Taken together, these data suggest that beta(3)-endonexin is phosphorylated by cyclinA/Cdk2 in vitro and that cyclin A-associated kinase activity is inhibited by the binding of beta(3)-endonexin to the kinase complex.     

Alzheimer beta-amyloid peptides: normal and abnormal localization

Alzheimer's disease (AD) neuropathology is characterized by accumulation of "senile" plaques (SPs) and neurofibrillary tangles (NFTs) in vulnerable brain regions. SPs are principally composed of aggregates of up to 42/43 amino acid beta-amyloid (A beta) peptides. The discovery of familial AD (FAD) mutations in the genes for the amyloid precursor protein (APP) and presenilins (PSs), all of which increase A beta42 production, support the view that A beta is centrally involved in the pathogenesis of AD. A beta42 aggregates readily, and is thought to seed the formation of fibrils, which then act as templates for plaque formation. A beta is generated by the sequential intracellular cleavage of APP by beta-secretase to generate the N-terminal end of A beta, and intramembranous cleavage by gamma-secretase to generate the C-terminal end. Cell biological studies have demonstrated that A beta is generated in the ER, Golgi, and endosomal/lysosomal system. A central question involving the role of A beta in AD concerns how A beta causes disease and whether it is extracellular A beta deposition and/or intracellular A beta accumulation that initiates the disease process. The most prevalent view is that SPs are composed of extracellular deposits of secreted A beta and that A beta causes toxicity to surrounding neurons as extracellular SP. The recent emphasis on the intracellular biology of APP and A beta has led some investigators to consider the possibility that intraneuronal A beta may directly cause toxicity. In this review we will outline current knowledge of the localization of both intracellular and extracellular A beta.     

Genetic characterization of Artemia tibetiana (Crustacea: Anostraca)

The brine shrimp Artemia consists of a number of bisexual species and a large number of parthenogenetic forms, which collectively, inhabit a wide range of hypersaline habitats. A recently described species (A. tibetiana) from a carbonate lake (Lagkor Co) in Tibet at an altitude of 4490 m has been tested with New World (A. franciscana USA, and A. franciscana feral population Vietnam) and Old World species (A. salina, A. urmiana, A. sinica) for cross fertility. These tests show complete infertility between A. tibetiana and A. franciscana . Between A. tibetiana and A. urmiana, A. sinica partial fertility through to F₂ and F₃ generations is evident. Allozyme and RAPD comparison of A. tibetiana with A. franciscana (USA), A. franciscana (Vietnam), A. sinica (Mongolia) and A. urmiana (Iran) show that A. tibetiana is similar to other bisexual species in mean heterozygosity (0.074) but has a somewhat higher proportion of polymorphic loci (40%, similar to that of A. urmiana ). The genetic distance between A. tibetiana and A. franciscana is 0.730, between A. tibetiana and A. urmiana is 0.475 and that between A. tibetiana and A. sinica is 0.114. F_IS estimates for A. tibetiana differ significantly from zero for six loci, mainly because of lack of fit to Hardy-Weinberg expectations. This may suggest that even within the limited area of Lagkor Co there are Genétically distinct populations. © 2002 The Linnean Society of London, Biological Journal of the Linnean Society , 2002, 75 , 333–344.     

Family study and frequency of blood group with strong B transferase accompanied by decreased A and H antigens

Subgroups of type A blood, named A1, A2, and A1-A2 intermediate (Aint), are specifically characterized by their peculiar A alleles and have their own A1-, A2- or Aint-forms of alpha-N-acetyl-D-galactosaminyltransferase (A-transferase). It is known, however, that certain type A2B persons exhibit A1-transferase. The reason may be an unusual alpha-galactosyltransferase (B-transferase). This strong B-transferase competes with A-transferase for the substrate, H antigen, so as to decrease the A and H antigens on the red cells. We studied this blood group over three generations and found that the strong B-transferase is, in fact, inherited with the B gene and is dominant over normal B-transferase. In AB blood groups in Tokyo, the frequency of people with a strong B-transferase is 5% for A1B and 22% for A2B. This enzyme does not always cause weak H or A antigens.     

The unique role of domain 2A of the hepatitis A virus precursor polypeptide P1-2A in viral morphogenesis

The initial step during assembly of the hepatitis A virus particle is driven by domain 2A of P1-2A, which is the precursor of the structural proteins. The proteolytic removal of 2A from particulate VP1-2A by an as yet unknown host enzyme presumably terminates viral morphogenesis. Using a genetic approach, we show that a basic amino acid residue at the C-terminus of VP1 is required for efficient particle assembly and that host proteases trypsin and cathepsin L remove 2A from hepatitis A virus particles in vitro. Analyses of insertion mutants in the C-terminus of 2A reveal that this part of 2A is important for liberation of P1-2A from the polyprotein. The data provide the first evidence that the VP1/2A junction is involved in both viral particle assembly and maturation and, therefore, seems to coordinate the first and last steps in viral morphogenesis.     

Contributions of the protein environment to the midpoint potentials of the A1 phylloquinones and the Fx iron-sulfur cluster in photosystem I

Electrostatic calculations have predicted that the partial negative charge associated with D575PsaB plays a significant role in modulating the midpoint potentials of the A1A and A1B phylloquinones in photosystem I. To test this prediction, the side chain of residue 575PsaB was changed from negatively charged (D) to neutral (A) and to positively charged (K). D566PsaB, which is located at a considerable distance from either A1A or A1B, and should affect primarily the midpoint potential of FX, was similarly changed. In the 575PsaB variants, the rate of electron transfer from A1A to FX is observed to decrease slightly according to the sequence D/A/K. In the 566PsaB variants, the opposite effect of a slight increase in the rate is observed according to the same sequence D/A/K. These results are consistent with the expectation that changing these residues will shift the midpoint potentials of nearby cofactors to more positive values and that the magnitude of this shift will depend on the distance between the cofactors and the residues being changed. Thus, the midpoint potentials of A1A and A1B should experience a larger shift than will FX in the 575PsaB variants, while FX should experience a larger shift than will either A1A or A1B in the 566PsaB variants. As a result, the driving energy for electron transfer from A1A and A1B to FX will be decreased in the former and increased in the latter. This rationalization of the changes in kinetics is compared with the results of electrostatic calculations. While the altered amino acids shift the midpoint potentials of A1A, A1B, and FX by different amounts, the difference in the shifts between A1A and FX or between A1B and FX is small so that the overall effect on the electron transfer rate between A1A and FX or between A1B and FX is predicted to be small. These conclusions are borne out by experiment.     

Two conformational states in the crystal structure of the Homo sapiens cytoplasmic ribosomal decoding A site

The decoding A site of the small ribosomal subunit is an RNA molecular switch, which monitors codon–anticodon interactions to guarantee translation fidelity. We have solved the crystal structure of an RNA fragment containing two Homo sapiens cytoplasmic A sites. Each of the two A sites presents a different conformational state. In one state, adenines A1492 and A1493 are fully bulged-out with C1409 forming a wobble-like pair to A1491. In the second state, adenines A1492 and A1493 form non-Watson–Crick pairs with C1409 and G1408, respectively while A1491 bulges out. The first state of the eukaryotic A site is, thus, basically the same as in the bacterial A site with bulging A1492 and A1493. It is the state used for recognition of the codon/anticodon complex. On the contrary, the second state of the H.sapiens cytoplasmic A site is drastically different from any of those observed for the bacterial A site without bulging A1492 and A1493.