Hybridization and introgression of the genomes of Drosophila nasuta and Drosophila albomicans: evolution of new karyotypes

Genome ◽  
2003 ◽  
Vol 46 (4) ◽  
pp. 605-611 ◽  
Author(s):  
M T Tanuja ◽  
N B Ramachandra ◽  
H A Ranganath
Keyword(s):  
Karyotype Evolution ◽  
Balancing Selection ◽  
Specific Effect ◽  
Directional Selection ◽  
Evolutionary Strategies ◽  
Transient Phase ◽  
Chromosomal Races ◽  
Drosophila Albomicans ◽  
Drosophila Nasuta ◽  
Hybridization And Introgression

Drosophila nasuta (2n = 8) and Drosophila albomicans (2n = 6) are cross-fertile allopatric sibling chromosomal races of the nasuta subgroup of Drosophila. Hybrids of these races can be maintained for any number of generations. Some of the introgressed hybrid lineages of D. nasuta and D. albomicans, after passing through a transient phase of karyotypic polymorphism, ended up with a stable karyotype whose composition is different from those of the parental races. Such hybrid populations were called cytoraces, in which the chromosomes of D. nasuta and D. albomicans are represented in different combinations. The karyotypic composition of 16 such cytoraces have been presented and discussed with reference to evolutionary strategies such as balancing selection, directional selection, and sex-specific effect on different components of the evolving karyotypes.Key words: Drosophila, nasuta, albomicans, hybridization, cytoraces, karyotype, evolution.

scholarly journals Balancing selection of the Intracellular Pathogen Response in natural Caenorhabditis elegans populations

2019 ◽  
Author(s):  
Lisa van Sluijs ◽  
Kobus J. Bosman ◽  
Frederik Pankok ◽  
Tatiana Blokhina ◽  
Joost A. G. Riksen ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Caenorhabditis Elegans ◽  
Balancing Selection ◽  
Model Organism ◽  
Evolutionary Strategies ◽  
Intracellular Pathogen ◽  
C Elegans ◽  
Pathogen Response ◽  
Orsay Virus ◽  
Selection Of

AbstractBackgroundGenetic variation in host populations may lead to differential viral susceptibilities. Here, we investigate the role of natural genetic variation present for an antiviral pathway, the Intracellular Pathogen Response (IPR), underlying susceptibility to Orsay virus in the model organism Caenorhabditis elegans. The IPR involves transcriptional activity of 80 genes including the pals-genes. The pals-genes form an expanded gene family which hints they could be shaped by an evolutionary selective pressure. Here we examine the genetic variation in the pals-family for traces of selection and explore the molecular and phenotypic effects of having distinct pals-gene alleles.ResultsGenetic analysis of 330 world-wide C. elegans strains reveals that genetic diversity within the IPR-related pals-genes can be categorized in a few haplotypes worldwide. Importantly, two key-IPR regulators, pals-22 and pals-25, are in a genomic region carrying signatures of balancing selection. Therefore, distinct pals-22/pals-25 alleles have been maintained in C. elegans populations over time, which suggests different evolutionary strategies exist in IPR regulation. We investigated the IPR by infecting two C. elegans strains that represent distinct pals-22/pals-25 haplotypes, N2 and CB4856, with Orsay virus to determine their susceptibility and transcriptional response to infection. Our data suggests that regulatory genetic variation underlies constant high activity of IPR genes in CB4856 which could determine the host transcriptional defense. We found that CB4856 shows initially lower viral susceptibility than N2. High basal IPR expression levels might help counteract viral infection directly, whereas N2-like strains that need to activate the IPR genes first may have a slower response. Nevertheless, most wild strains harbor N2-like alleles for the pals-genes.ConclusionsOur work provides evidence for balancing genetic selection of immunity genes in C. elegans and illustrated how this may shape the transcriptional defense against pathogens. The transcriptional and genetic data presented in this study therefore provide a novel perspective on the functional diversity that can develop within a main antiviral response in natural host populations.

scholarly journals POPULATION GENETICS OF DROSOPHILA NASUTA NASUTA, DROSOPHILA NASUTA ALBOMICANA AND THEIR HYBRIDS. I. KARYOTYPIC MOSAICISM IN THE HYBRID POPULATIONS

Genetics ◽  
1979 ◽  
Vol 93 (1) ◽  
pp. 211-215
Author(s):  
M R Rajasekarasetty ◽  
L Siddaveere Gowda ◽  
N B Krishnamurthy ◽  
H A Ranganath
Keyword(s):  
Population Genetics ◽  
Chromosomal Races ◽  
Drosophila Nasuta ◽  
Drosophila Nasuta Nasuta

ABSTRACT D. n. nasuta and D. n. albomicana constitute a pair of chromosomal races with 2n=8 and 2n=6, respectively. The F1 of these has 2n=7 and it is fertile. There exists a state of karyotypic mosaicism as evidenced by the presence of 26 types of chromosome combinations in F2, F3, and F10 populations. In the midst of this karyotypic noise, the karyotype similar to that of F1 reached 51% of the population. Implications of these findings are discussed.

scholarly journals Distinct evolutionary strategies of human leucocyte antigen loci in pathogen-rich environments

2012 ◽  
Vol 367 (1590) ◽  
pp. 830-839 ◽  
Author(s):  
Alicia Sanchez-Mazas ◽  
Jean-François Lemaître ◽  
Mathias Currat
Keyword(s):  
Genetic Diversity ◽  
Genetic Drift ◽  
Human Leucocyte Antigen ◽  
Balancing Selection ◽  
Allelic Diversity ◽  
Hla Class I ◽  
Significant Negative Correlation ◽  
Evolutionary Strategies ◽  
Hla Genes ◽  
Geographical Distances

Human leucocyte antigen (HLA) loci have a complex evolution where both stochastic (e.g. genetic drift) and deterministic (natural selection) forces are involved. Owing to their extraordinary level of polymorphism, HLA genes are useful markers for reconstructing human settlement history. However, HLA variation often deviates significantly from neutral expectations towards an excess of genetic diversity. Because HLA molecules play a crucial role in immunity, this observation is generally explained by pathogen-driven-balancing selection (PDBS). In this study, we investigate the PDBS model by analysing HLA allelic diversity on a large database of 535 populations in relation to pathogen richness. Our results confirm that geographical distances are excellent predictors of HLA genetic differentiation worldwide. We also find a significant positive correlation between genetic diversity and pathogen richness at two HLA class I loci (HLA-A and -B), as predicted by PDBS, and a significant negative correlation at one HLA class II locus (HLA-DQB1). Although these effects are weak, as shown by a loss of significance when populations submitted to rapid genetic drift are removed from the analysis, the inverse relationship between genetic diversity and pathogen richness at different loci indicates that HLA genes have adopted distinct evolutionary strategies to provide immune protection in pathogen-rich environments.

Autoradiographic study of transcription and dosage compensation in the sex and neo-sex chromosome of Drosophila nasuta nasuta and Drosophila nasuta albomicans

Genome ◽  
2001 ◽  
Vol 44 (1) ◽  
pp. 71-78 ◽  
Author(s):  
G Mahesh ◽  
N B Ramachandra ◽  
H A Ranganath
Keyword(s):  
X Chromosome ◽  
Dosage Compensation ◽  
Sex Chromosomes ◽  
Sex Chromosome ◽  
Autoradiographic Study ◽  
The Other ◽  
Chromosomal Races ◽  
Heteromorphic Sex Chromosomes ◽  
Drosophila Nasuta ◽  
Drosophila Nasuta Nasuta

Cellular autoradiography is used to study the transcription patterns of the polytene X chromosomes in Drosophila nasuta nasuta and D. n. albomicans. D. n. nasuta, with 2n = 8, includes a pair of complete heteromorphic sex chromosomes, whereas D. n. albomicans, with 2n = 6, has a pair of metacentric neo-sex chromosomes representing incomplete heteromorphic sex chromosomes. The neo-X chromosome has two euchromatic arms, one representing the ancestral X while the other represents the ancestral autosome 3 chromosomes. The metacentric neo-Y chromosome has one arm with a complete heterochromatic ancestral Y and the other arm with a euchromatic ancestral autosome 3. The transcription study has revealed that the X chromosome in D. n. nasuta is hyperactive, suggesting complete dosage compensation, while in the neo-X chromosome of D. n. albomicans the ancestral X chromosome is hyperactive and the ancestral autosome 3, which is part of the neo-sex chromosome, is similar to any other autosomes. This finding shows dosage compensation on one arm (XLx/–) of the neo-X chromosome, while the other arm (XR3/YR3) is not dosage compensated and has yet to acquire the dosage compensatory mechanism.Key words: Drosophila, chromosomal races, neo-sex chromosome, transcription and dosage compensation.

scholarly journals Major histocompatibility complex selection dynamics in pathogen-infected túngara frog ( Physalaemus pustulosus ) populations

2016 ◽  
Vol 12 (8) ◽  
pp. 20160345 ◽  
Author(s):  
Tiffany A. Kosch ◽  
Arnaud Bataille ◽  
Chelsea Didinger ◽  
John A. Eimes ◽  
Sofia Rodríguez-Brenes ◽  
...  
Keyword(s):  
Genetic Variation ◽  
Major Histocompatibility Complex ◽  
Mhc Class Ii ◽  
Balancing Selection ◽  
Directional Selection ◽  
Major Histocompatibility ◽  
Physalaemus Pustulosus ◽  
Mhc Ii ◽  
Histocompatibility Complex ◽  
Selection Dynamics

Pathogen-driven selection can favour major histocompatibility complex (MHC) alleles that confer immunological resistance to specific diseases. However, strong directional selection should deplete genetic variation necessary for robust immune function in the absence of balancing selection or challenges presented by other pathogens. We examined selection dynamics at one MHC class II (MHC-II) locus across Panamanian populations of the túngara frog, Physalaemus pustulosus , infected by the amphibian chytrid fungus Batrachochytrium dendrobatidis (Bd). We compared MHC-II diversity in highland túngara frog populations, where amphibian communities have experienced declines owing to Bd, with those in the lowland region that have shown no evidence of decline. Highland region frogs had MHC variants that confer resistance to Bd. Variant fixation appeared to occur by directional selection rather than inbreeding, as overall genetic variation persisted in populations. In Bd-infected lowland sites, however, selective advantage may accrue to individuals with only one Bd-resistance allele, which were more frequent. Environmental conditions in lowlands should be less favourable for Bd infection, which may reduce selection for specific Bd resistance in hosts. Our results suggest that MHC selection dynamics fluctuate in túngara frog populations as a function of the favourability of habitat to pathogen spread and the vulnerability of hosts to infection.

The Effect of Vitamin A on the Intermittent Nitrogen Dioxide Gas Exposure in Hamsters

1976 ◽  
Vol 34 ◽  
pp. 176-177
Author(s):  
J.C.S. Kim ◽  
M.G. Jourden ◽  
E.S. Carlisle
Keyword(s):  
Electron Microscopy ◽  
Vitamin A ◽  
Nitrogen Dioxide ◽  
Chronic Exposure ◽  
Light And Electron Microscopy ◽  
Specific Effect ◽  
Deficient Diet ◽  
Intermittent Exposure ◽  
Hypovitaminosis A ◽  
Gas Exposure

Chronic exposure to nitrogen dioxide in rodents has shown that injury reaches a maximum after 24 hours, and a reparative adaptive phase follows (1). Damage occurring in the terminal bronchioles and proximal portions of the alveolar ducts in rats has been extensively studied by both light and electron microscopy (1).The present study was undertaken to compare the response of lung tissue to intermittent exposure to 10 ppm of nitrogen dioxide gas for 4 hours per week, while the hamsters were on a vitamin A deficient diet. Ultrastructural observations made from lung tissues obtained from non-gas exposed, hypovitaminosis A animals and gas exposed animals fed a regular commercially prepared diet have been compared to elucidate the specific effect of vitamin A on nitrogen dioxide gas exposure. The interaction occurring between vitamin A and nitrogen dioxide gas has not previously been investigated.

Platelet-Bound Prekallikrein Promotes Pro-Urokinase-Induced Clot Lysis: A Mechanism for Targeting the Factor XII Dependent Intrinsic Pathway of Fibrinolysis

1994 ◽  
Vol 71 (03) ◽  
pp. 347-352 ◽  
Author(s):  
Jean-Pierre Loza ◽  
Victor Gurewich ◽  
Michael Johnstone ◽  
Ralph Pannell
Keyword(s):  
Platelet Rich Plasma ◽  
Specific Inhibitor ◽  
Specific Effect ◽  
Clot Lysis ◽  
Factor Xii ◽  
Intrinsic Pathway ◽  
Clot Retraction ◽  
Enzymatic Mechanism ◽  
Low Concentrations ◽  
Factor Xiia

SummaryClots formed from platelet rich plasma were found to be lysed more readily by low concentrations of pro-urokinase (pro-UK) than clots formed from platelet poor plasma. This was not a non-specific effect since the reverse occurred with tissue plasminogen activator. A mechanical explanation due to platelet-mediated clot retraction was excluded by experiments in which retraction was inhibited with cyto-chalasin B. Therefore, a platelet-mediated enzymatic mechanism was postulated to explain the promotion of fibrinolysis. Casein autography of isolated platelets revealed a ≈ 90 kDa band of activity which comigrated with plasma prekallikrein (PK)/kallikrein, a known activator of pro-UK. Furthermore, treatment of platelets with plasma PK activator (PPA), consisting essentially of factor XIIa, induced activation of pro-UK and of chromomgenic substrate for kallikrein (S-2302). This activity corresponded to approximately 40-200 pM kallikrein per 10 8 washed and gel filtered platelets per ml. The activation of pro-UK by PPA-pretreated platelets was dose-dependent and inhibited by soybean trypsin inhibitor but not by bdellin, a specific inhibitor of plasmin, nor by the corn inhibitor of factor XIIa. Kinetic analysis of pro-UK activation by kallikrein showed promotion of the reaction by platelets. The KM of the reaction was reduced by platelets by ≈ 7-fold, while the kcat was essentially unchanged. In conclusion, PK was shown to be tightly associated with platelets where it can be activated by factor XIIa during clotting. The activation of pro-UK by platelet-bound kallikrein provides an explanation for the observed platelet mediated promotion of pro-UK-induced clot lysis. Since pro-UK and plasminogen have also been shown to be associated with platelets, the present findings suggest a mechanism by which the factor Xlla-dependent intrinsic pathway of fibrinolysis can be localized and targeted to a thrombus.

The Effects of Heparin and Annexin V on Fibrin Accretion after Injury in the Jugular Veins of Rabbits

1993 ◽  
Vol 69 (03) ◽  
pp. 227-230 ◽  
Author(s):  
J Van Ryn-McKenna ◽  
H Merk ◽  
T H Müller ◽  
M R Buchanan ◽  
W G Eisert
Keyword(s):  
Vessel Wall ◽  
Thrombin Generation ◽  
Antithrombin Iii ◽  
Specific Effect ◽  
Annexin V ◽  
Inhibitory Effect ◽  
Jugular Veins ◽  
Prothrombinase Complex ◽  
Wall Injury

SummaryWe compared the relative abilities of unfractionated heparin and annexin V to prevent fibrin accretion onto injured jugular veins in vivo. Heparin was used to accelerate the inhibition of thrombin by antithrombin III, and annexin V was used to inhibit the assembly of the prothrombinase complex on phospholipid surfaces, thereby blocking thrombin generation. Rabbit jugular veins were isolated in situ, a 2 cm segment was injured by perfusing it with air, and then blood flow was re-established. Five minutes later, each rabbit was injected with heparin (20 U/kg) or annexin V (0.3 mg/kg) and then with 125I-fibrinogen. The amount of 125I-fibrin accumulation onto each injured vessel wall segment was measured 4 h later. Each injured vessel was completely deendothelialized as a result of the air perfusion as demonstrated by electron microscopy. 125I-fibrin accretion onto the injured jugular veins was enhanced 2.4-fold as compared to the uninjured veins in sham-operated animals. Heparin treatment did not reduce fibrin accretion, whereas, annexin V treatment decreased fibrin accretion by 60%, p <0.05. This latter effect was achieved without sustained circulating anticoagulation. Additional experiments confirmed that the inhibitory effect of annexin V on fibrin accretion was associated with a surface specific effect, since more annexin V bound to the injured jugular vein segments as compared to the non-injured jugular veins. We conclude that, i) mild vessel wall injury (selective de-endothelialization) in veins results in a thrombogenic vessel wall; ii) the thrombogenecity of which is not inhibited by prophylactic doses of heparin; but iii) is inhibited by annexin V, which binds to injured vessel wall surface, and inhibits thrombin generation independently of antithrombin III.

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