QUANTITATIVE VARIATION IN FINITE PARTHENOGENETIC POPULATIONS: WHAT STOPS MULLER'S RATCHET IN THE ABSENCE OF RECOMBINATION?

Finite parthenogenetic populations with high genomic mutation rates accumulate deleterious mutations if back mutations are rare. This mechanism, known as Muller's ratchet, can explain the rarity of parthenogenetic species among so called higher organisms. However, estimates of genomic mutation rates for deleterious alleles and their average effect in the diploid condition in Drosophila suggest that Muller's ratchet should eliminate parthenogenetic insect populations within several hundred generations, provided all mutations are unconditionally deleterious. This fact is inconsistent with the existence of obligatory parthenogenetic insect species. In this paper an analysis of the extent to which compensatory mutations can counter Muller's ratchet is presented. Compensatory mutations are defined as all mutations that compensate for the phenotypic effects of a deleterious mutation. In the case of quantitative traits under stabilizing selection, the rate of compensatory mutations is easily predicted. It is shown that there is a strong analogy between the Muller's ratchet model of Felsenstein (1974) and the quantitative genetic model considered here, except for the frequency of compensatory mutations. If the intensity of stabilizing selection is too small or the mutation rate too high, the optimal genotype becomes extinct and the population mean drifts from the optimum but still reaches a stationary distribution. This distance is essentially the same as predicted for sexually reproducing populations under the same circumstances. Hence, at least in the short run, compensatory mutations for quantitative characters are as effective as recombination in halting the decline of mean fitness otherwise caused by Muller's ratchet. However, it is questionable whether compensatory mutations can prevent Muller's ratchet in the long run because there might be a limit to the capacity of the genome to provide compensatory mutations without eliminating deleterious mutations at least during occasional episodes of sex.     

THE CHROMOSOMES OF PARTHENOGENETIC FROGS AND TADPOLES

1. This paper presents cytological observations upon Dr. Loeb''s parthenogenetic frog material, with considerations upon the mechanism by which the diploid number and both sexes may be produced. 2. Both sexes of adults and tadpoles are present. 3. The chromosome number is diploid and probably 26 in both sexes. Sex chromosomes cannot be distinguished. 4. The chromosome numbers observed by other authors in parthenogenetic frog material are haploid, diploid, and variable. Their significance is considered. 5. The mechanism producing the diploid number, based on European observations, appears to be a doubling of the haploid number at some time after the second polar body is given off. 6. Overripeness may be a factor in producing both sexes of parthenogenetic frogs and tadpoles. 7. Genetic data indicate that the normal male is digametic and that there are differences of potency between male and female factors for sex which vary in frogs of the two races and in strains within the race. These differences have been interpreted by Witschi as forming a series of multiple allelomorphs.     

THE PRODUCTION OF PARTHENOGENETIC MAMMALIAN EMBRYOS AND THEIR USE IN BIOLOGICAL RESEARCH

1. The eggs of many mammalian species show signs of early parthenogenetic development as they age after ovulation and oocytes may form transplantable terato-carcinomas. These cases of apparently spontaneous parthenogenetic development suggest that the cells of the female germ line have an inherent tendency to divide and differentiate. 2. The ovulated eggs of virgin female mammals may be stimulated to start parthenogenetic development by a wide variety of treatments. Most of these damage the egg so that it does not develop beyond the 4 cell stage. However if the eggs are exposed to electrical activation, hyaluronidase treatment, or temperature shock then in many cases they will develop into blastocysts. 3. These blastocysts may be either haploid or diploid. Haploid blastocysts may be formed either by the egg extruding the nucleus of the second polar body or by the egg dividing in half, so that the female pronucleus is in one cell and the nucleus of the second polar body is in another cell. Diploid blastocysts are formed by the retention of the nucleus of the second polar body within the egg. The way in which the egg develops may be controlled by altering the osmolarity of the culture medium, the age of the egg at the time of activation, or the strain of animal used. 4. The action of the sperm on the egg can be defined by comparing the events of normal fertilization and parthenogenetic activation. Both these stimuli cause the egg to expose binding sites for Concanavalin A to synthesize DNA and to divide. However, the release of cortical granules, which occurs after fertilization, does not appear to be induced by parthenogenetic activation, and it is significant that parthenogenones lack the sperm nucleus and mitochondria. 5. The majority of parthenogenones die soon after implantation. Death at this time occurs with parthenogenones obtained from the activated eggs of both inbred and outbred stocks. Death might be caused by recessive lethal mutations or by extra-genetic effects of the maternal chromosomes. 6. Parthenogenones contain endogenous A-type particles which shows that these bodies are inherited through the female germ line. 7. Parthenogenones may in the future provide both a method for chromosome mapping and a source of haploid cells. At present the use of mammalian parthenogenones in biological research is restricted by the heavy embryonic losses which occur around the time of implantation. This means that the role of the sperm, gene activity and virus expression must be studied during a very limited period. Part of the mortality before implantation is the consequence of the damage which the egg suffers during activation and it should be possible to reduce this loss by improving the techniques for activation. It may also be possible to increase the quantity of cells derived from haploid and diploid mammalian embryos by deriving teratocarcinomas from them.     

FOUNDER EFFECTS AND THE RATE OF MITOCHONDRIAL DNA EVOLUTION IN HAWAIIAN DROSOPHILA

The nearly-neutral-mutation theory predicts that populations with small effective sizes will undergo more rapid molecular evolution than populations with very large effective sizes. In particular, Ohta (1976) predicted that populations of Hawaiian Drosophila that are known to have small population sizes and to experience repeated population bottlenecks due to founder events should show a more rapid rate of molecular evolution relative to the rate of molecular evolution of species with large population sizes such as the continental Drosophila. In this paper we test this prediction by comparing the rate of molecular evolution in two closely related lineages of Hawaiian Drosophila that have experienced very different evolutionary histories. Both lineages belong to the planitibia subgroup of Hawaiian Drosophila. The beta lineage (which includes D. silvestris, D. planitibia, D. differens, and D. hemipeza) has undergone repeated founder events, as evidenced by their geographic distribution and behavioral biology. On the other hand, evidence on geographic distribution and behavior indicates that the alpha lineage (which includes D. melanocephala, D. cyrtaloma, and D. neoperkinsi) has arisen from large ancestral populations without founder effects. The mitochondrial DNA data reveal that, within a lineage, the rate of molecular evolution is rather uniform, while all comparisons between the two lineages show that the rate of molecular evolution in the beta lineage is three times that of the alpha lineage. This analysis strongly supports the predictions made by Ohta.     

6-DMAP对小鼠卵母细胞减数分裂启动及孤雌发育作用

小鼠卵泡卵母细胞体外培养过程中加入2 mmol/L 6-DMAP可抑制卵母细胞自发的染色质浓缩和生发泡破裂(GVBD)。源自超排的MⅡ期卵母细胞则能为6-DMAP所激活。hCG注射后18—19h的卵母细胞置于2 mmol/L6-DMAP的CZB溶液中培养0.5 h、1h、2h、3h,卵母细胞的激活率分别为26.1%、75.2%、75.8%、77.3%、;卵裂率分别为88.2%、73.2%、67.0%、58.4%。与乙醇激活法相比,6-DMAP处理引起了不同的孤雌激活类型。     

CHROMOSOME NUMBERS OF HAWAIIAN FLOWERING PLANTS AND THE SIGNIFICANCE OF CYTOLOGY IN SELECTED TAXA

Chromosome numbers are reported for 128 species of flowering plants indigenous or endemic to Hawaii, including first reports for 13 genera and 82 species. The special significance of reports for Ilex, Tribulus, Keysseria, Pisonia, Boerhavia, Jacquemontia, Claoxylon, Lipochaeta, Railliardia, and Dubautia are discussed. The cytological and morphological variation in Railliardia and Dubautia is considered and their treatment as congeners is advocated. The cytogeogruphic pattern in Dubautia and Railliardia and other factors suggest that the ancestral chromosome number of the Hawaiian tarweeds is n = 14. Their derivation from a western North American progenitor similar to Adenothamnus is considered plausible if not indeed likely.     

应用氯化锶和放线菌酮对小鼠卵母细胞进行孤雌活化的研究

本试验研究了SrCl_2浓度和作用时间,以及卵龄和蛋白合成抑制剂放线菌酮等对昆明种小鼠卵母细胞活化的影响。研究表明,以含1.6mmol/L SrCl_2的无钙M16液对小鼠卵母细胞活化效果最好(87.0％),显著(P<0.05)优于SrCl_2浓度为1.0、5.0、10.0mmol/L的同种液体。SrCl_2作用时间10分钟显著(P<0.05)好于5、20、30或60分钟。注射hCG后18和20小时卵母细胞的活化率(分别为87.0％和84.6％)显著(P<0.01)高于14或16小时的活化率(分别为4.8％和16.5％)。CHX与SrCl_2联合使用产生显著的协同促进卵母细胞活化作用。     

DIFFERENTIATION AND INTEGRATION OF THE GENOME IN POPULATIONS OF THE MARINE COPEPOD TIGRIOPUS CALIFORNICUS

Geographically separated populations of the intertidal copepod Tigriopus californicus are sharply differentiated at several enzyme-encoding gene loci. Two studies were performed to investigate the extent to which the gene pools of local populations are organized into harmoniously interacting (or “coadapted”) gene complexes. In the first, the effects of interpopulation hybridization on development time were assessed. Results showed that while F₁ hybrids did not differ from parental lines, mean F₂ developmental times were as much as 50% longer. The second study used two unlinked enzyme polymorphisms as genetic markers to determine the genotypic specificity of F₂ hybrid breakdown. For two sets of parental populations, the relative viabilities of the different two-locus genotypes were determined from segregation ratios among the F₂ progeny. Sharp deviations from Mendelian ratios were observed; in the extreme, a block of genes marked by the Me^F allozyme from the LJ (La Jolla) population was found to be nearly lethal when homozygous in the F₂ of LJ × AB (Los Angeles) crosses. This same block of genes had a tenfold higher viability in crosses between LJ and SC (Santa Cruz). In the AB × LJ crosses, the two marker loci had independent (multiplicative) effects on viability. In the SC × LJ crosses, deviations from the multiplicative model were observed; the data indicate that parental homozygous genotypes have higher viability than predicted by independence, while nonparental homozygotes have lower than predicted viability. These results suggest that substantial integration of the genome has occurred within natural T. californicus populations.