Evidence from mitochondrial DNA that African honey bees spread as continuous maternal lineages

African honey bees have populated much of South and Central America and will soon enter the United States. The mechanism by which they have spread is controversial. Africanization may be largely the result of paternal gene flow into extant European populations or, alternatively, of maternal migration of feral swarms that have maintained an African genetic integrity. We have been using both mitochondrial and nuclear DNA restriction fragment length polymorphisms to follow the population dynamics between European and African bees. In earlier reports, we suggested that if African honey bees had distinctive mitochondrial (mt) DNA, then it could potentially distinguish the relative contributions of swarming and mating to the Africanization process. Because mtDNA is maternally inherited, it would not be transmitted by mating drones and only transported by queens accompanying swarms. Furthermore, the presence of African mtDNA would reflect unbroken maternal lineages from the original bees introduced from Africa. The value of mtDNA for population studies in general has been reviewed recently. Here we report that 19 feral swarms, randomly caught in Mexico, all carried African mtDNA. Thus, the migrating force of the African honey bee in the American tropics consists of continuous African maternal lineages spreading as swarms. The mating of African drones to European queens seems to contribute little to African bee migration.     

蜜蜂生物节律研究进展

 生物节律主要指有机体生命活动的内在节律性。蜜蜂生物节律受到其社会性的影响,从而参与许多复杂行为的调控。与果蝇相比,蜜蜂的生物节律与哺乳动物更相似。工蜂和蜂王的生物节律表现出高度的可塑性。例如,工蜂的昼夜节律受其劳动分工形式的调控,并通过与幼蜂的直接接触来调节,哺育蜂昼夜照料幼虫,在行为或时钟基因表达方面没有昼夜节律变化。从蜜蜂的社会性、蜜蜂生物节律产生的分子机制、神经基础、研究方法、可塑性、蜜蜂的睡眠等方面综述了蜜蜂生物节律的研究进展。     

Deletions of muscle mitochondrial DNA in patients with mitochondrial myopathies

In vitro studies of muscle mitochondrial metabolism in patients with mitochondrial myopathy have identified a variety of functional defects of the mitochondrial respiratory chain, predominantly affecting complex I (NADH-CoQ reductase) or complex III (ubiquinol-cytochrome c reductase) in adult cases. These two enzymes consist of approximately 36 subunits, eight of which are encoded by mitochondrial DNA (mtDNA). The increased incidence of maternal, as opposed to paternal, transmission in familial mitochondrial myopathy suggests that these disorders may be caused by mutations of mtDNA. Multiple restriction endonuclease analysis of leukocyte mtDNA from patients with the disease, and their relatives, showed no differences in cleavage patterns between affected and unaffected individuals in any single maternal line. When muscle mtDNA was studied, nine of 25 patients were found to have two populations of muscle mtDNA, one of which had deletions of up to 7 kilobases in length. These observations demonstrate that mtDNA heteroplasmy can occur in man and that human disease may be associated with defects of the mitochondrial genome.     

Conformational mutations in human mitochondrial DNA

Variation in the human mitochondrial DNA (mtDNA) sequence has been extensively analysed using restriction fragment length polymorphisms (RFLPs). MtDNA RFLPs have previously been attributed to nucleotide changes within restriction endonuclease recognition sites or to small insertion-deletion mutations. We now report that RFLPs detected by polyacrylamide gel electrophoresis can also result from single nucleotide substitutions which alter the mobility of small- to medium-sized restriction fragments that incorporate the sequence. We have defined the mutation responsible at two loci and have identified several possible additional loci. When screening human mtDNAs with multiple restriction endonucleases, such mutations can be misidentified as insertion-deletion mutations or counted as multiple polymorphic restriction sites. This can lead to errors in constructing restriction maps and estimating sequence diversity.     

Complete replacement of mitochondrial DNA in Drosophila

The introduction of foreign mitochondria or mitochondrial DNA into a cell is a useful technique for clarifying the molecular mechanisms responsible for the maintenance of mitochondria. Novel combinations of mitochondrial and nuclear genomes have been studied in mammalian cells in culture and in yeast. In Drosophila, we have recently constructed heteroplasmic flies possessing both endogenous mitochondrial DNA and foreign mitochondrial DNA by intra- and interspecific transplantation of germ plasm. During the maintenance of these heteroplasmic lines, flies of D. melanogaster are produced that no longer possess their own mitochondrial DNA but retain the foreign mitochondrial DNA from D. mauritiana. .These flies are fertile and the foreign mitochondrial DNA is stably maintained in their offspring. Here we report the complete replacement of endogenous mitochondrial DNA with that from another multicellular species. Molecular and genetic analysis of this replacement in Drosophila should provide new insight into the functional interaction between nuclear and organelle genomes.     

Paternal inheritance of mitochondrial DNA in mice.

For nearly 20 years it has been assumed on the basis of low-resolution experiments that mitochondrial (mt)DNA, in contrast to the genes in the nucleus, has an exclusively maternal mode of inheritance in animals. Using the polymerase chain reaction, paternally inherited mtDNA molecules have now been detected in mice at a frequency of 10(-4), relative to the maternal contributions. These mice were hybrids between two inbred strains (C57BL/6J and Mus spretus) whose mtDNAs can be distinguished easily. This new mode of inheritance provides a mechanism for generating heteroplasmy and may explain mitochondrial disorders exhibiting biparental transmission.     

Premature ageing in mice expressing defective mitochondrial DNA polymerase

Point mutations and deletions of mitochondrial DNA (mtDNA) accumulate in a variety of tissues during ageing in humans, monkeys and rodents. These mutations are unevenly distributed and can accumulate clonally in certain cells, causing a mosaic pattern of respiratory chain deficiency in tissues such as heart, skeletal muscle and brain. In terms of the ageing process, their possible causative effects have been intensely debated because of their low abundance and purely correlative connection with ageing. We have now addressed this question experimentally by creating homozygous knock-in mice that express a proof-reading-deficient version of PolgA, the nucleus-encoded catalytic subunit of mtDNA polymerase. Here we show that the knock-in mice develop an mtDNA mutator phenotype with a threefold to fivefold increase in the levels of point mutations, as well as increased amounts of deleted mtDNA. This increase in somatic mtDNA mutations is associated with reduced lifespan and premature onset of ageing-related phenotypes such as weight loss, reduced subcutaneous fat, alopecia (hair loss), kyphosis (curvature of the spine), osteoporosis, anaemia, reduced fertility and heart enlargement. Our results thus provide a causative link between mtDNA mutations and ageing phenotypes in mammals.     

中国白兔线粒体DNA限制性图谱

用 ６ 种限制性内切酶分析了中国白兔的线粒体 Ｄ Ｎ Ａ（ｍ ｔ Ｄ Ｎ Ａ）。测得其相对分子质量约为１６．８, Ｅｃｏ ＲⅤ, Ｂａｍ ＨⅠ, ＰｓｔⅠ, Ｅｃｏ ＲⅠ, ＨｉｎｄⅢ在中国白兔 ｍ ｔ Ｄ Ｎ Ａ 上分别有 １,２,２,２,６ 个切点, ＳａｌⅠ 在其上没有切点。根据单酶降解和双酶降解片段的相对分子质量,构建了中国白兔ｍ ｔ Ｄ Ｎ Ａ的限制性内切酶图谱。     

Energetic cost of carrying loads: have African women discovered an economic way?

When travelling in East Africa one is often surprised at the prodigious loads carried by the women of the area. It is not uncommon to see women of the Luo tribe carrying loads equivalent to 70% of their body mass balanced on the top of their heads (Fig. 1). Women of the Kikuyu tribe carry equally large loads supported by a strap across their foreheads; this frequently results in a permanently grooved skull. Recent experiments on running horses, humans, dogs and rats showed that the energy expended in carrying a load increased in direct proportion to the weight of the load for each animal at each speed, that is, carrying a load equal to 20% of body weight increased the rate of energy consumption by 20% (ref. 1). The purpose of the present study was to determine whether these African women use specialized mechanisms for carrying very large loads cheaply. We found that both the Luo and Kikuyu women could carry loads of up to 20% of their body weight without increasing their rate of energy consumption. For heavier loads there was a proportional increase in energy consumption, that is, a 30% load increased energy consumption by 10%, a 40% load by 20% and so on. We suggest that some element of training and/or anatomical change since childhood may allow these women to carry heavy loads economically.