英帕纤恙螨和吉首纤恙螨生活史的研究

本文报道了实验室饲养下对英帕纤恙螨和吉首纤恙螨生活史的观察结果。在月平均室温22.6～32.1℃及饱和相对湿度并供给充分食物条件下,从卵发育至成虫英帕纤恙螨需23～100天,平均44.5天,吉首纤恙螨22～107天,平均49.3天。完成一代所需时间英帕纤恙螨平均57.5天,吉首纤恙螨57.8天。1只雄螨一生产精孢量英帕纤恙螨190～2423枚,平均每天产8.9枚,吉首纤恙螨137～1161枚,平均每天产5.5枚。1只雌螨一生产卵量英帕纤恙螨143～306个,平均每天产卵10.4个,吉首纤恙螨214～510个,平均每天产卵17.7个。     

绒螨目线粒体基因组研究进展

绒螨目是一个数量庞大且分散的类群,许多绒螨目螨类具有医学和经济学意义。本文从线粒体基因组的一般结构及基因重排、蛋白质编码基因、rRNA基因、tRNA基因、控制区、系统发育关系六个方面对绒螨目螨类线粒体基因组进行回顾,综述了当前已测序的绒螨目螨类线粒体基因组,系统总结了近年来报道的绒螨目线粒体全序列的基因特征、绒螨目的系统发育关系。     

云南省小板纤恙螨形态学研究北大核心CSCD

目的通过与文献记载的福建省小板纤恙螨(福建株)和日本小板纤恙螨(日本株)对比,了解云南省小板纤恙螨(云南株)形态学变异情况。方法从云南省宾川县采集到的小板纤恙螨标本,选取形态完好和结构清晰的100只,在显微镜下观察和测量其背板、背板附属结构及其他身体参数,将测量数据与福建省小板纤恙螨和日本小板纤恙螨进行比较分析。结果云南株小板纤恙螨背板的AW、PW、SB、ASB、PSB、SD、AP、AM、AL、PL、S值范围较福建株大,其中PW、SB、PSB、AM及PW/SD、PW/AP测量均值大于福建小板纤恙螨(均P<0.01),ASB、SD、AL、PL测量均值小于福建株(均P<0.01)。福建株小板纤恙螨幼虫的体长测量范围较宽,幼虫3对足长度的均值均大于云南株(均P<0.01)。云南株小板纤恙螨背板的AW、PW、SB、ASB、PSB、SD、AP、AM、AL、PL、S值范围较日本株大,其中AW、PW、ASB、AP、SD、AM、AL、PL以及身体参数pa、pm、pp、Ip测量均值小于日本株小板纤恙螨(均P<0.01)。结论与福建小板纤恙螨(福建株)和日本小板纤恙螨(日本株)相比,云南株小板纤恙螨存在一定的形态学变异,可能存在地理种群的分化。     

云南省小型哺乳动物寄生恙螨群落研究

目的探讨云南省恙螨的群落结构及生物多样性特征。方法选取云南省16个县（市）为调查点，现场用鼠笼加食饵诱捕小型哺乳动物（小兽），收集耳廓和外耳道全部恙螨，常规分类、鉴定。恙螨的群落结构与生物多样性特征分别用香浓-威纳（Shannon-Wiener）指数（多样性和均匀性指数）、辛普森（Simpson）多样性指数、丰富性指数和优势指数分析。结果捕获小兽6888只，属5目10科26属，在双耳部检获恙螨共87416只，属3亚科21属192种，存在9种优势恙螨。宿主动物寄生恙螨的多样性与丰富性指数依次为啮齿目〉食虫目〉攀驹目。各生境群落中，丰富性指数与多样性指数山区森林灌丛〉山区耕地室内〉坝区草甸耕地〉坝区室内房周。优势指数均较低。9种优势恙螨种类的生态位宽度依次为寒冬纤恙螨0．81，乡野纤恙螨0．57，小板纤恙螨0．52，绒鼠纤恙螨0．51，中华纤恙螨0．42，西盟合轮恙螨0，39，枪棒爬虫恙螨0．39，树驹纤恙螨0．27，副须纤恙螨0．04，其中任意两螨种间的生态位重叠指数在0～0．54间。群落内主要恙螨种类的空间分布呈聚集型。结论云南省恙螨群落结构复杂，物种多样性较高，群落内主要恙螨种类呈聚集型分布，优势恙螨的生态位宽度与生态位重叠差异均明显。     

纤恙螨属一新种(蜱螨亚纲:恙螨科)

本描述纤恙螨属Ｌｅｐｔｏｔｒｏｍｂｉｄｉｕｍ Ｎａｇａｙｏ ｅｔ ａｌ,１９１６一新种,徐氏纤恙螨Ｌｅｐｔｏｔｒｏｍｂｉｄｉｕｍ ｈｓｕｉ ｓ．ｎｏｖ。模式标本存放在青海省地方病防治研究所。     

云南省主要鼠类寄生恙螨群落研究

目的 了解云南省优势鼠种寄生恙螨群落结构及其生物多样性。 方法 选取云南省16个县（市）为调查点，现场用鼠笼加食饵诱捕小兽，收集其耳廓和外耳道全部恙螨，进行分类、鉴定。恙螨的群落结构与生物多样性特征分别用香浓?鄄维纳（Shannon-Wiener）指数（多样性和均匀性指数）、丰富性指数和优势指数分析。 结果 有7种优势鼠种其双耳部检获恙螨共52 151只, 属3亚科17属131种，Shannon-Wiener多样性指数趋势依次为褐家鼠＞齐氏姬鼠＞大绒鼠＞锡金小鼠＞大足鼠＞黄胸鼠＞卡氏小鼠，丰富性指数与均匀性指数的趋势与此基本一致。6种优势恙螨种类的生态位宽度依次为枪棒爬虫恙螨＞小板纤恙螨＞中华纤恙螨＞西盟合轮恙螨＞寒冬纤恙螨＞绒鼠纤恙螨，其中任意两螨种间的生态位重叠指数均大于0.76。各优势恙螨的种间关系较复杂，部分种类之间有程度不同的、较轻微的正协调关系。 结论 云南省主要鼠种体表恙螨群落结构复杂，物种多样性较高。优势恙螨的生态位宽度差异与生态位重叠均明显。     

高湖纤恙螨为媒介的恙虫病160例临床分析

1957年魏晋举氏在我区青田高湖乡进行恙虫病调查中,发现一新种恙螨,定名为高湖纤恙螨,经一系列的观察与研究确认该螨为我国恙虫病的新媒介,且证实我区是以高湖纤恙螨为媒介的恙虫病新疫区。恙虫病在我区每年均有流行。现将近年来我区地、市两家医院确诊并有较完整记录的160例,恙虫病综合分析     

福建近年恙螨感染恙虫病东方体的检测研究

目的　检测恙螨幼虫体内恙虫病东方体, 分析福建恙虫病可能流行的趋势。方法　从福建山区及沿海地区捕鼠采集恙螨幼虫, 通过分类鉴定, 以每只鼠体的寄生螨作为一个被检单位, 用套式 Ｐ Ｃ Ｒ 扩增恙虫病东方体 Ｓｔａ ５８ｋ Ｄａ 基因的８８ｂｐ 片段, 以确定恙螨幼虫是否携带本病原, 继而估计该地区是否存在恙虫病疫源地。结果　从１０５ 份被检单位的恙螨幼虫检出７ 份恙虫病东方体阳性标本, 主要宿主为黄毛鼠, 主要媒介为纤恙螨属的地里纤及小板纤恙螨, 与有关资料比较,证实本省恙虫病的宿主和媒介未发生明显变化。结论　福建沿海地区恙螨的恙虫病东方体的感染率高于山区, 疫源地有继续扩大的趋势。     

云南省16县（市）大绒鼠体表寄生恙螨调查

目的 了解云南省大绒鼠体表寄生恙螨的种类、空间分布情况、优势种及其种间关系。 方法 选取2000～2004年云南省16县（市）现场用鼠笼加食饵诱捕大绒鼠,收集耳壳及耳窝部所有恙螨,进行分类和鉴定。恙螨种间关系与种群的空间分布格局分别用协调系数（V）和聚块指数（m*/m）判定。 结果 捕获大绒鼠1 157只。收集恙螨37 613只,隶属3亚科9 属80种。大绒鼠总带螨率（68.2%）和总螨指数（32.5）较高,其中小板纤恙螨、中华纤恙螨、西盟合轮恙螨、绒鼠纤恙螨、枪棒爬虫恙螨、寒冬纤恙螨6种恙螨为优势种,在不同大绒鼠个体之间呈聚集型分布;优势恙螨之间存在正协调和负协调关系。 结论 大绒鼠体表恙螨种类繁多、数量大、物种多样性高,主要恙螨在大绒鼠体表的寄生有聚集性。     

用PCR检测现场单个小盾纤恙螨体内恙虫病立克次体的研究

恙虫病立克次体表面蛋白５６ＫＤａ基因编码区构建的群特异引物，采用嵌合式聚合酶链反应检测现场捕获的单个小盾纤恙螨幼虫体内Ｒ．ｔ的ＤＮＡ。共检测江苏省恙虫病疫区小盾纤恙螨幼虫６１只，结果２只幼虫提取的ＤＮＡ经扩增后见４８１￣５０７ｂｐ的ＤＮＡ扩增带，表明这２只幼虫携带有Ｒ．ｔ，其该种螨Ｒ．ｔ携带率为３．２７％，证明该法可用于单个恙螨幼虫体的Ｒ．ｔ的检测，对恙虫病疫区媒介恙螨的流行病学调查具有实用价值。     

欧亚鸲特鲁螨线粒体tRNA基因重新注释与分析

目的 验证欧亚鸲特鲁螨(Trouessartia rubecula)线粒体基因组中是否存在tRNA基因的丢失,并以此过程为基础提出一套完整的无气门股螨类线粒体基因组t RNA基因注释流程,为螨类线粒体基因组tRNA基因注释提供参考。方法 联合MITOS、tRNAscan-SE、MITOS2和ARWEN等多个tRNA注释软件预测欧亚鸲特鲁螨线粒体tRNA基因,结合人工序列检查、人工手动查找以及可能二级结构的最小自由能(minimum free energy, MFE)进行验证。结果 利用MITOS和ARWEN的预测结果结合人工序列修正,重新注释欧亚鸲特鲁螨线粒体基因组中“缺失”的trn E、trn I和trn Y基因,人工手动查找到trn A和trn V基因。重新注释的欧亚鸲特鲁螨线粒体基因组具有22个tRNA基因,不存在tRNA基因的丢失。结论 在注释无气门亚目中螨类线粒体时,为了获得更加准确的tRNA基因注释结果,应广泛运用tRNA基因预测程序,并且对预测结果进行人工检查和修正,以期减少单一程序预测以及注释程序预测方法所导致的偏差。     

Shaping and reshaping of salmonid genomes by amplification of tRNA-derived retroposons during evolution.

Three families of tRNA-derived repeated retroposons in the genomes of salmonid species have been isolated and characterized. These three families differ in sequence, but all are derived from a tRNA(Lys) or from a tRNA species structurally related to tRNA(Lys). The salmon Sma I family is present in the genomes of two species of the genus Oncorhynchus but not in other species, including five other species of the same genus. The charr Fok I family is present only in four species and subspecies of the genus Salvelinus. The third family, the salmonid Hpa I family, appears to be present in all salmonid species but is not present in species that are not members of the Salmonidae. Thus, the genome of proto-Salmonidae was originally shaped by amplification and dispersion of the salmonid Hpa I family and then reshaped by amplification of the Sma I and Fok I families in the more recently evolved species of salmon and charr, respectively. We speculate that amplification and dispersion of retroposons may have played a role in salmonid speciation.     

A homoplasmic mitochondrial transfer ribonucleic acid mutation as a cause of maternally inherited hypertrophic cardiomyopathy

OBJECTIVES: The purpose of this study was to understand the clinical and molecular features of familial hypertrophic cardiomyopathy (HCM) in which a mitochondrial abnormality was strongly suspected. BACKGROUND: Defects of the mitochondrial genome are responsible for a heterogeneous group of clinical disorders, including cardiomyopathy. The majority of pathogenic mutations are heteroplasmic, with mutated and wild-type mitochondrial deoxyribonucleic acid (mtDNA) coexisting within the same cell. Homoplasmic mutations (present in every copy of the genome within the cell) present a difficult challenge in terms of diagnosis and assigning pathogenicity, as human mtDNA is highly polymorphic. METHODS: A detailed clinical, histochemical, biochemical, and molecular genetic analysis was performed on two families with HCM to investigate the underlying mitochondrial defect. RESULTS: Cardiac tissue from an affected child in the presenting family exhibited severe deficiencies of mitochondrial respiratory chain enzymes, whereas histochemical and biochemical studies of the skeletal muscle were normal. Mitochondrial DNA sequencing revealed an A4300G transition in the mitochondrial transfer ribonucleic acid (tRNA)(Ile) gene, which was shown to be homoplasmic by polymerase chain reaction/restriction fragment length polymorphism analysis in all samples from affected individuals and other maternal relatives. In a second family, previously reported as heteroplasmic for this base substitution, the mutation has subsequently been shown to be homoplasmic. The pathogenic role for this mutation was confirmed by high-resolution Northern blot analysis of heart tissue from both families, revealing very low steady-state levels of the mature mitochondrial tRNA(Ile). CONCLUSIONS: This report documents, for the first time, that a homoplasmic mitochondrial tRNA mutation may cause maternally inherited HCM. It highlights the significant contribution that homoplasmic mitochondrial tRNA substitutions may play in the development of cardiac disease. A restriction of the biochemical defect to the affected tissue has important implications for the screening of patients with cardiomyopathy for mitochondrial disease.     

Codon recognition rules in yeast mitochondria.

The mitochondrial genome of Saccharomyces cerevisiae codes for 24 tRNAs. The nucleotide sequences of the tRNA genes suggest a unique set of rules that govern the decoding of the mitochondrial genetic code. The four codons of unmixed fmilies are recognized by single tRNAs that always have a U in the wobble position of the anticodon. The codons of the mixed families are read by two different tRNAs. Codons terminating in a C or U are recognized by tRNAs with a G and codons terminating in a G or A are recognized by tRNAs with a U in the corresponding positions of the anticodons. There are two exceptions to these rules. In the AUN family for isoleucine and methionine, the isoleucine tRNA has a G and the methionine tRNA has a C in the wobble position. The tRNA for the arginine CGN family also has an A in the wobble position of the anticodon. It is of interest that the CGN codons have not been found in the mitochondrial genes sequenced to date. The simplified decoding system of yeast mitochondria allows all the codons to be recognized by only 24 tRNAs.     

In vitro reconstruction of the mitochondrial translation system of yeast.

We have isolated the translation system from yeast mitochondria and have reconstructed it in vitro. This submitochondrial system, composed of mitochondrial ribosomes, tRNA, pH 5 fraction and mRNA, is maximally active at 10 mM Mg2+ and 100 mM KCl or NH4Cl. NH4+ is more stimulatory than K+. Added Escherichia coli tRNA gives less than half the activity obtained with added mitochondrial tRNA. Activity is enhanced with protease inhibitors but not with Ca2+, spermine, or spermidine. In contrast to heterologous translation systems, the present system produces products with molecular weights similar to those of products synthesized by yeast mitochondria in vivo and by intact yeast mitochondria in vitro. The results support the idea that the unique coding features of the mitochondrial genome require a unique translation system for accurate translation of mitochondrial mRNAs.     

Mitochondrial genome mutations in hypertensive individuals

Human essential hypertension (HTN), a polygenic, multifactorial, and highly heterogeneous disorder of unknown etiology, has been shown to have excess maternal transmission in several studies, suggesting a possible mitochondrial involvement. In an effort to assess the contribution of the mitochondrial genome to HTN we initiated a systematic, extended screening of hypertensive individuals to identify potentially pathogenic mtDNA mutations. We applied our newly developed novel class of tests for the detection of mitochondrial mutation involvement in complex diseases to the hypertension data set from 350 pedigrees of white ethnicity and 98 of African American ethnicity ascertained at HTN clinics associated with Boston Medical Center, and we identified families with a likely mitochondrial involvement. We analyzed the sequence of the entire mitochondrial genome in probands from 20 such pedigrees, consisting of 10 African American and 10 white families. Comparison with the reference "Cambridge" sequence revealed a total of 297 base changes, including 24 in the ribosomal RNA (rRNA) genes, 15 in the transfer RNA (tRNA) genes, and 46 amino acid substitutions, with the remainder involving the noncoding regions or synonymous changes. Among the coding region mutations, 30 are novel, with 13 hypertensive probands carrying at least one novel variant, usually in combination with the previously described common polymorphisms, several of which are associated with cardiovascular and renal pathologies. These data will serve as a starting point for large-scale case-control association studies.     

Mammalian mitochondria have the innate ability to import tRNAs by a mechanism distinct from protein import

Mitochondrial genomes generally encode a minimal set of tRNAs necessary for protein synthesis. However, a number of eukaryotes import tRNAs from the cytoplasm into their mitochondria. For instance, Saccharomyces cerevisiae imports cytoplasmic tRNA(Gln) into the mitochondrion without any added protein factors. Here, we examine the existence of a similar active tRNA import system in mammalian mitochondria. We have used subcellular RNA fractions from rat liver and human cells to perform RT-PCR with oligonucleotide primers specific for nucleus-encoded tRNA(CUG)(Gln) and tRNA(UUG)(Gln) species, and we show that these tRNAs are present in rat and human mitochondria in vivo. Import of in vitro transcribed tRNAs, but not of heterologous RNAs, into isolated mitochondria also demonstrates that this process is tRNA-specific and does not require the addition of cytosolic factors. Although this in vitro system requires ATP, it is resistant to inhibitors of the mitochondrial electrochemical gradient, a key component of protein import. tRNA(Gln) import into mammalian mitochondria proceeds by a mechanism distinct from protein import. We also show that both tRNA(Gln) species and a bacterial pre-tRNA(Asp) can be imported in vitro into mitochondria isolated from myoclonic epilepsy with ragged-red fiber cells if provided with sufficient ATP (2 mM). This work suggests that tRNA import is more widespread than previously thought and may be a universal trait of mitochondria. Mutations in mitochondrial tRNA genes have been associated with human disease; the tRNA import system described here could possibly be exploited for the manipulation of defective mitochondria.     

Fine-scale mergers of chloroplast and mitochondrial genes create functional,transcompartmentally chimeric mitochondrial genes

The mitochondrial genomes of flowering plants possess a promiscuous proclivity for taking up sequences from the chloroplast genome. All characterized chloroplast integrants exist apart from native mitochondrial genes, and only a few, involving chloroplast tRNA genes that have functionally supplanted their mitochondrial counterparts, appear to be of functional consequence. We developed a novel computational approach to search for homologous recombination (gene conversion) in a large number of sequences and applied it to 22 mitochondrial and chloroplast gene pairs, which last shared common ancestry some 2 billion years ago. We found evidence of recurrent conversion of short patches of mitochondrial genes by chloroplast homologs during angiosperm evolution, but no evidence of gene conversion in the opposite direction. All 9 putative conversion events involve the atp1/atpA gene encoding the alpha subunit of ATP synthase, which is unusually well conserved between the 2 organelles and the only shared gene that is widely sequenced across plant mitochondria. Moreover, all conversions were limited to the 2 regions of greatest nucleotide and amino acid conservation of atp1/atpA. These observations probably reflect constraints operating on both the occurrence and fixation of recombination between ancient homologs. These findings indicate that recombination between anciently related sequences is more frequent than previously appreciated and creates functional mitochondrial genes of chimeric origin. These results also have implications for the widespread use of mitochondrial atp1 in phylogeny reconstruction.