scholarly journals The mechanism whereby the genes M1 and M2 in Paramecium aurelia, stock 540, control growth of the mate-killer (mu) particles

1962 ◽  
Vol 3 (1) ◽  
pp. 24-50 ◽  
Author(s):  
I. Gibson ◽  
G. H. Beale ◽  
E. C. R Reeve
Keyword(s):  
Recipient Cell ◽  
Physiological Activity ◽  
Dominant Gene ◽  
Initial Number ◽  
Irregular Distribution ◽  
Large Numbers ◽  
Control Growth ◽  
Phenotypic Manifestation ◽  
A Cell ◽  
Dominant Genes

1. Replacement of the dominant genes M1 and M2 in Paramecium aurelia, stock 540 (syngen/variety 1), results in loss of ability to maintain mu particles and manifestation of mate-killing after a delay of eight to fifteen fissions in most cells. The change, when it does occur, is relatively abrupt, extending over less than the space of one inter-fission period.2. The delay between change of genotype and loss of mu particles is interpreted as being due to presence in the initial cytoplasm of some thousand ‘metagons’, which are non-replicating gene derivatives having the physiological activity of the corresponding genes. During successive fissions of paramecia deprived of M1 and M2 the metagons are passively distributed amongst the progeny, until virtually all animals lack them.3. On reaching a stage at which some individuals of genotype m1m1m2m2 contain only a single metagon, the paramecia still contain large numbers of mu particles and are mate-killers. Fission of such animals gives rise to one daughter again with mu particles, and another in which the latter are destroyed during the next inter-fission period.4. By induced cytoplasmic exchange between conjugants, metagons can be transferred from one animal to another via the cytoplasm. Where such transference is into an animal not originally containing mu particles, that animal is converted into a condition in which it favours the maintenance of mu particles and transmits the latter to one or more of its offspring.5. Distribution of metagons amongst progeny of dividing paramecia is not random, due possibly to clumping of the metagons. Induced cytoplasmic exchange seems to break up the clumps.6. Reintroduction of a dominant gene (M2) into a cell recently deprived of the same gene, succeeds—even after fifteen fissions—in re-establishing the ability to support growth of mu particles, provided that the recipient cell contains at least one metagon and one or more mu particles. There is a regular lag of only one fission between introduction of such a dominant gene and its phenotypic manifestation.7. Mathematical formulae are developed for calculating the expected initial number of metagons, the proportions of animals lacking mu particles at each fission following loss of the dominant genes, and the proportions of cells containing 0, 1, 2 …, etc. metagons per cell at any stage. The consequences of one of the possible types of irregular distribution of metagons in dividing paramecia are also considered mathematically.

scholarly journals A Stochastic Model for Virus Growth in a Cell Population

2014 ◽  
Vol 51 (3) ◽  
pp. 599-612 ◽  
Author(s):  
J. E. Björnberg ◽  
T. Britton ◽  
E. I. Broman ◽  
E. Natan
Keyword(s):  
Stochastic Model ◽  
Host Cell ◽  
Cell Population ◽  
Branching Process ◽  
Virus Population ◽  
Virus Growth ◽  
Optimal Balance ◽  
Large Numbers ◽  
A Cell

In this work we introduce a stochastic model for the spread of a virus in a cell population where the virus has two ways of spreading: either by allowing its host cell to live and duplicate, or by multiplying in large numbers within the host cell, causing the host cell to burst and thereby let the virus enter new uninfected cells. The model is a kind of interacting Markov branching process. We focus in particular on the probability that the virus population survives and how this depends on a certain parameter λ which quantifies the ‘aggressiveness’ of the virus. Our main goal is to determine the optimal balance between aggressive growth and long-term success. Our analysis shows that the optimal strategy of the virus (in terms of survival) is obtained when the virus has no effect on the host cell's life cycle, corresponding to λ = 0. This is in agreement with experimental data about real viruses.

scholarly journals How environment shapes horizontal gene transfer

2020 ◽  
Vol 2 (7A) ◽  
Author(s):  
Rama Bhatia ◽  
Hande Kirit ◽  
Jonathan Bollback
Keyword(s):  
Gene Transfer ◽  
Horizontal Gene Transfer ◽  
Gene Dosage ◽  
Recipient Cell ◽  
Endogenous Gene ◽  
Fitness Effects ◽  
Serovar Typhimurium ◽  
A Cell ◽  
Evolutionary Fate

The evolutionary fate of a horizontal gene transfer (HGT) event is determined by its fitness on the recipient cell, i.e., whether it is beneficial, neutral or deleterious. The distribution of fitness effects (DFE), thus is a fundamental predictor of the outcome of an HGT event. The environment plays a considerable role in determining the fitness cost of a horizontally transferred gene. We have studied the fitness effects of genes transferred from Salmonella enterica serovar Typhimurium to Escherichia coli in six environments, that potentially represent the conditions experienced by the two species. The data suggests high variability of genes in different environments. Genes, whose fitness varies substantially between environments, may be able to persist in populations while being deleterious in one environment, they may be neutral or even beneficial in another environment, suggesting that environmental fluctuations may increase the likelihood of HGT. In addition to the in vitro environments, we are also looking at, how changes in the intrinsic environment of a cell, after an HGT event, could affect fitness. An increase in protein dosage due to functional similarity of the horizontally transferred gene to the endogenous gene can cause an imbalance in the cell, thereby leading to a negative fitness effect. By comparing the growth rates of each ortholog gene with the wild type strain, we can elucidate when gene dosage acts as a barrier to HGT.

INHERITANCE OF CROWN RUST RESISTANCE IN THREE ACCESSIONS OF AVENA STERILIS

1980 ◽  
Vol 22 (1) ◽  
pp. 27-33 ◽  
Author(s):  
D. E. Harder ◽  
R. I. H. McKenzie ◽  
J. W. Martens
Keyword(s):  
Rust Resistance ◽  
Dominant Gene ◽  
Crown Rust ◽  
Inheritance Of Resistance ◽  
Single Dominant Gene ◽  
Avena Sterilis ◽  
Oat Crown Rust ◽  
Crown Rust Resistance ◽  
Resistance Spectrum ◽  
Dominant Genes

The inheritance of resistance to oat crown rust was studied in three accessions of Avena sterilis L. Accession CAV 4274 originated from Morocco, CAV 4540 from Algeria, and CAV 3695 from Tunisia. Seedling rust tests on F2 backcross families indicated the presence of two dominant genes for crown rust resistance in CAV 4274. One of these, a gene conditioning resistance to most races tested, was linked or allelic to gene Pc-38, and was designated gene Pc-62. The second gene conferred resistance only to one of the six races studied, and was not tested further. In CAV 4540, a single dominant gene, Pc-63 was possibly allelic with Pc-62 and linked or allelic to Pc-38. Genes Pc-62 and 63 are generally similar to Pc-38 in their resistance spectrum, but these three genes are differentiated by races CR 102, CR 103, and CR 107. A single dominant gene in CAV 3695 appeared to be Pc-50.

THE INHERITANCE OF LOOSE SMUT RESISTANCE.: I. THE INHERITANCE OF RESISTANCE IN FOUR BARLEY VARIETIES IMMUNE TO RACE 2 OF LOOSE SMUT

1962 ◽  
Vol 42 (1) ◽  
pp. 69-77 ◽  
Author(s):  
E. N. Larter ◽  
H. Enns
Keyword(s):  
Disease Resistance ◽  
Dominant Gene ◽  
The Other ◽  
Inheritance Of Resistance ◽  
Single Dominant Gene ◽  
Loose Smut ◽  
Race 2 ◽  
Or Genes ◽  
Dominant Genes

Four barley varieties, each immune to a Valki-attacking culture of loose smut (designated as race 2), were studied with respect to the inheritance of their resistance. Jet (C.I. 967) and Nigrinudum (C.I. 2222) were each found to possess two independent dominant genes determining resistance. Steudelli (C.I. 2266) proved to be immune to race 2 through the action of a single dominant gene, while resistance of Hillsa (C.I. 1604) was found to be conditioned by two complementary dominant genes. The absence of susceptible F3 families in crosses between Jet, Nigrinudum, and Steudelli indicated that these three varieties have in common a gene or genes for resistance to the race of smut used. The two complementary genes for resistance in Hillsa proved to be distinct from those of the other three varieties under study.The use of genetic analyses of disease resistance based upon classification of F3 families of the backcross to the resistant source is described and the merits of such a method are discussed.

The inheritance of resistance to Puccinia coronata and of floret characters in Avena sterilis

1983 ◽  
Vol 25 (4) ◽  
pp. 329-335 ◽  
Author(s):  
L. S. L. Wong ◽  
R. I. H. McKenzie ◽  
D. E. Harder ◽  
J. W. Martens
Keyword(s):  
Rust Resistance ◽  
Dominant Gene ◽  
Crown Rust ◽  
Puccinia Coronata ◽  
Inheritance Of Resistance ◽  
Avena Sterilis ◽  
Field Isolates ◽  
Crown Rust Resistance ◽  
Dominant Genes

The inheritance of resistance to Puccinia coronata, awn development, lemma pubescence, and lemma color were studied in the Avena sterilis accessions CAV 4248, CAV 4656, and CAV 4904. Three independent, partially dominant genes (Pc-64, Pc-65, Pc-66) in CAV 4248, one partially dominant gene (Pc-67) in CAV 4656, and a dominant gene (Pc-68) in CAV 4904 were identified which conferred resistance to P. coronata. Genes Pc-64, Pc-65, Pc-66, Pc-67, and Pc-68 conferred resistance to 13, 8, 6, 12, and 14 races, respectively, of the 14 races of P. coronata tested. Gene Pc-68 conferred resistance to all field isolates of P. coronata collected in Canada in 1981 and was found to be closely linked or allelic to gene Pc-46. Awns and lemma pubescence were inherited monogenically in crosses with all three CAV accessions. Grey lemma color was controlled by one gene in CAV 4248 and by two genes in CAV 4656. Brown lemma color was controlled by one gene, which was closely linked or pleiotropic with the gene for lemma pubescence in CAV 4904. There was no association between crown rust resistance and the three floret characters studied.

Development of Active-Cells for Macroscopically Deformable Structures

2014 ◽  
Author(s):  
Ahsan I. Nawroj ◽  
John P. Swensen ◽  
Aaron M. Dollar
Keyword(s):  
Shape Memory ◽  
Composite Structures ◽  
Electrical Current ◽  
Conceptual Structure ◽  
Prior Work ◽  
Connected Network ◽  
Cell Structures ◽  
Large Numbers ◽  
Structural Deformations ◽  
A Cell

In this paper we describe extensions and improvements upon prior work on “active cells” — small contractile electromechanical elements used in large numbers to create actuated composite structures. Each element (cell) consists of square fiberglass end-pieces encapsulating a bias spring within two telescoping tubes, actuated using two contractile shape memory coils, and occupying approx. 1cm3 when fully contracted. The end-pieces contain conductive interfaces to nearby cells, thus allowing channeling of power through a connected network of cells to provide actuation far from the source of electrical current. Prior work developed the conceptual structure of such a cell as well as preliminary prototypes. This paper describes the attachment of cells to each other and to rapid-prototyped cell interconnects — as well as improved fabrication techniques for the shape-memory coils — resulting in robust actuation for each cell, and the creation of considerably more complex chained and networked composite structures. A detailed exploration of appropriate interconnect mechanisms, powering schemes to provide network-level structural deformations, and examples of multi-cell structures are presented.

scholarly journals SIMILARITY OF THE KINETICS OF INVERTASE ACTION IN VIVO AND IN VITRO. III

1933 ◽  
Vol 16 (4) ◽  
pp. 571-577 ◽  
Author(s):  
J. M. Nelson ◽  
B. G. Wilkes
Keyword(s):  
Physiological Activity ◽  
Water Concentration ◽  
Invertase Activity ◽  
Yeast Cells ◽  
Identical Manner ◽  
A Cell ◽  
Relationship Of ◽  
The Relationship

1. The relationship of sucrose and water concentration to invertase activity in vivo and in vitro has been studied under the same environmental conditions. 2. The sucroclastic activity of S. cerevisiae cells and of invertase solutions prepared from them reacts to changes in sucrose and water concentration in an identical manner. 3. The invertase contained in living yeast cells is just as freely exposed to the conditions of sucrose and water concentrations of the suspending medium as it would be if it were contained in a cell-free solution. Weight is added to the previous suggestion (2) that yeast invertase exerts its physiological activity in a region quite close to the surface of the cell.

scholarly journals The Inheritance and Association of Rust (Uromyces apendiculatus) Resistance and Foliar Abnormalities in Phaseolus vulgaris L.

HortScience ◽  
1995 ◽  
Vol 30 (4) ◽  
pp. 823A-823
Author(s):  
J.M. Bokosi ◽  
D.P. Coyne ◽  
J.R. Steadman ◽  
D. O'Keefe ◽  
J. Reiser
Keyword(s):  
Phaseolus Vulgaris ◽  
Specific Resistance ◽  
Dominant Gene ◽  
Hybrid Plant ◽  
Single Dominant Gene ◽  
Phaseolus Vulgaris L ◽  
Recessive Genes ◽  
Dominant Genes

The inheritance of specific resistance (SR) and foliar abnormalities (FA) were studied in the F2 and F3 progeny of the following crosses; `PC-50' × Chichara 83-10, `PC-50' × `EZ Pick', A-10-2 × GN `Beryl', and A-10-2 × P114. A single dominant gene controlled SR to rust strain US85NP10-1 in `PC-50' × Chichara 83-10. Duplicate recessive genes determined foliar crippling (FC) in `PC-50' × Chichara 83-10 and A-10-2 × P114. The inheritance of hybrid plant abnormality in `PC-50' × `EZ Pick' and A-10-2 × GN `Beryl' differed from previously reported complementary dominant genes or duplicate recessive genes. Foliar variegation (FV) was controlled by duplicate recessive genes in `PC-50' × Chichara 83-10 and by triplicate recessive genes in `PC-50' × `EZ Pick', A-10-2 × GN `Beryl', and A-10-2 × P114. No associations were detected between SR and FC, SR and FV, or FC and FV.

scholarly journals Study of Inheritance and Linkage of Virulence Genes in a Selfing Population of a Pakistani Dominant Race of Puccinia striiformis f. sp. tritici

2020 ◽  
Vol 21 (5) ◽  
pp. 1685 ◽  
Author(s):  
Sajid Mehmood ◽  
Marina Sajid ◽  
Syed Kamil Husnain ◽  
Jie Zhao ◽  
Lili Huang ◽  
...  
Keyword(s):  
Stripe Rust ◽  
Puccinia Striiformis ◽  
Single Gene ◽  
Dominant Gene ◽  
Wheat Varieties ◽  
Parental Isolate ◽  
The One ◽  
Almost All ◽  
Simple Sequence ◽  
Dominant Genes

Wheat stripe rust is a severe threat of almost all wheat-growing regions in the world. Being an obligate biotrophic fungus, Puccinia striiformis f. sp. tritici (PST) produces new virulent races that break the resistance of wheat varieties. In this study, 115 progeny isolates were generated through sexual reproduction on susceptible Himalayan Berberis pseudumbellata using a dominant Pakistani race (574232) of PST. The parental isolate and progeny isolates were characterized using 24 wheat Yr single-gene lines and ten simple sequence repeat (SSR) markers. From the one-hundred-and-fifteen progeny isolates, 25 virulence phenotypes (VPs) and 60 multilocus genotypes were identified. The parental and all progeny isolates were avirulent to Yr5, Yr10, Yr15, Yr24, Yr32, Yr43, YrSp, YrTr1, YrExp2, Yr26, and YrTye and virulent to Yr1, Yr2, Yr6, Yr7, Yr8, Yr9, Yr17, Yr25, Yr27, Yr28, YrA, Yr44, and Yr3. Based on the avirulence/virulence phenotypes, we found that VPs virulent to Yr1, Yr2, Yr9, Yr17, Yr47, and YrA were controlled by one dominant gene; those to YrSp, YrTr1, and Yr10 by two dominant genes; and those to YrExp2 by two complementary dominant genes. The results are useful in breeding stripe rust-resistant wheat varieties and understanding virulence diversity.

Artificial APC-Based Generation of IL-21 Secreting CD4+ T Cells That Can Provide Help to CD8+ T Cells.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 466-466
Author(s):  
Makito Tanaka ◽  
Marcus Butler ◽  
Sascha Ansén ◽  
Osamu Imataki ◽  
Alla Berezovskaya ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Binding Assay ◽  
Cell Responses ◽  
Large Numbers ◽  
A Cell

Abstract Abstract 466 CD8+ T cells are thought to be major players in T cell immunity because of their potent direct effector function. However, many studies have demonstrated that CD4+ T cells also play a critical role by providing help which optimizes CD8+ T cell responses. In vivo experiments using murine models have suggested that common cytokine receptor γ-chain cytokines such as IL-2, IL-15 and IL-21 are mediators of this CD4+ T cell help. Previously, we generated K562-based artificial APC (aAPC) by transducing HLA-A2, CD80, and CD83. This aAPC can generate large numbers of antigen-specific CD8+ CTL with a central/effector memory phenotype and potent effector function. These CTL are surprisingly long-lived and can be maintained in vitro without any feeder cells or cloning. We are currently conducting a clinical trial where large numbers of anti-tumor CD8+ CTL generated ex vivo using this aAPC and IL-2/IL-15 are adoptively transferred to patients with advanced cancer. Early results have demonstrated that adoptively transferred anti-tumor CTL can expand and persist as memory T cells for longer than 6 months without lymphodepletion or cytokine administration. Furthermore, some patients have demonstrated objective clinical responses. These in vivo results suggest that K562-based aAPC might serve as a clinically important APC to generate large numbers of antigen-specific T cells for adoptive therapy. Based upon these observations, we have generated a K562-derived aAPC that can expand antigen-specific CD4+ T cells capable of providing help to CD8+ T cells. One challenge with the study of human HLA class II-restricted antigen-specific CD4+ T cells lies in the fact that there is no DR allele with a frequency greater than 25% in any race or ethnic extraction. To overcome this issue, we targeted HLA-DP0401 (DP4), which is positive in 64% of Caucasians and is the most frequent HLA allele in many other ethnic groups. aAPC was generated by sequentially transducing DPA1*0103, DPB1*0401, CD80 and CD83 to HLA class I-, class II-, CD54+, CD58+ K562. Using this aAPC and 57 overlapping peptides encompassing the full-length protein, we identified three DP4-restricted immunogenic epitopes derived from CMV pp65. One of the 3 epitopes, peptide #23 (aa 221-240) appeared to be an immunodominant epitope, since specific CD4+ T cells were expanded from all donors tested. A cell-based in vitro competitive binding assay confirmed that #23 binds DP4 molecules. #23-specific CD4+ T cells generated using aAPC and low dose IL-2/IL-15 were long-lived, up to 4 months in vitro without any feeder cells or cloning, and were able to recognize APC exogenously pulsed with pp65 protein. ELISPOT showed that #23-specific CD4+ T cells were able to secrete IL-2, IL-4, IFN-γbut not IL-10 in an antigen-specific manner. Interestingly, intracellular cytokine staining revealed that a fraction of IFN-γsecreting CD4+ T cells concurrently produced IL-4. Most importantly, using an aAPC expressing HLA-A2, DP4, CD80, and CD83, we were able to demonstrate that pp65-specific CD4+ T cells can provide help to pp65-specific CD8+ T cells in an antigen-specific way. Survivin is an attractive target antigen for tumor immunotherapy, since it is expressed by many tumor types and is indispensable for tumor growth. We have also successfully generated DP4-restricted Survivin-specific CD4+ T cells using this aAPC. Using a cell-based in vitro binding assay, 5 Survivin-derived peptides with high binding capacity to DP4 molecules were identified. Among these 5 peptides, peptide #90 (aa 90-104) bound DP4 most potently. aAPC pulsed with #90 was able to induce antigen-specific CD4+ T cell responses from cancer patients. These CD4+ T cells were also long-lived, up to 3 months in vitro and secreted IL-2, IL-4, and IFN-γbut not IL-10. Interestingly, IL-21 was also produced upon antigen-specific stimulation. It should be noted that our K562-based aAPC did not expand Foxp3+ regulatory T cells under the experimental conditions tested. Taken all together, we have established a K562-based aAPC to generate large numbers of HLA-DP4-restricted antigen-specific CD4+ T cells that possess longevity and functional competence. Based upon our previous success in clinical translation of K562-based aAPC for CD8+ T cells and the high prevalence of HLA-DP4, generating a clinical grade version of this aAPC for CD4+ T cells is of high priority. Disclosures: No relevant conflicts of interest to declare.

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