scholarly journals Extra cytoproct mutant inParamecium tetraurelia: a genetical study

1976 ◽  
Vol 27 (2) ◽  
pp. 143-159 ◽  
Author(s):  
Stephen F. Ng

SUMMARYThe basis of inheritance of the extra cytoproct (XP) character inParamecium tetraurelia, stock d4-154, is shown to be nuclear and probably a single dominant gene,Ec, with reduced penetrance in heterozygotes. When the mutant gene is replaced by its wild-type allele, loss of the XP phenotype in some lines of descent occurs before 15 cell generations, but in more than half of the lines this occurs after 15–120 or more cell generations. The possibility is considered that these extremely long and variable ‘lags’ may be due to extranuclear (cortical) inheritance of cortical changes initially produced by gene action.

Development ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 125-137
Author(s):  
Mark S. Ellinger

A mutant gene, Pale, (Pa) has been discovered in the discoglossid frog, Bombina orientalis. Breeding experiments indicate that the gene is recessive to the wild-type allele (P). Embryos, tadpoles and adults homozygous for the Pale gene are lighter in coloration than wild-type animals. Eggs produced by Pale females appear normally pigmented. Neural-retina defects were apparent in Pale tadpoles. Parabiosis experiments revealed that the Pale and wild-type phenotypes were unaffected by circulating factors from the opposite phenotype. Neuralcrest-grafting experiments revealed that Pale melanophores retain the Pale phenotype when placed in a wild-type cellular environment. Likewise, wild-type chromatophores are unaffected by residence in Pale tissues. Melanophores of Pale tadpoles display reduced numbers of mature melanosomes. This is the primary morphological basis of the Pale phenotype. However, other chromatophore classes (xanthophores, iridophores) were also less intensely pigmented, demonstrating that a single gene may affect the pigmentation of all chromatophore classes in B. orientalis.


1976 ◽  
Vol 27 (2) ◽  
pp. 123-134 ◽  
Author(s):  
James D. Berger

SUMMARYA study of the patterns of phenotypic change in exconjugants using the recessive behavioural mutant pawn (pwA) and its wild-type allele shows that both cytoplasmic and nuclear factors contribute to phenomic lag. Following loss of the wild-type allele from the macronucleus, phenomic lag lasts for 6–11 cell cycles in various sublines of a single clone. Inherited cytoplasmic material is estimated to be responsible for phenomic lag of no more than 5–6 cell cycles. Longer persistence of the parental phenotype is due to continued gene activity in macronuclear fragments carrying the wild-type allele. Genes in fragments remain active and can result in maintenance of the parental phenotype as long as fragments are present (up to 11 cell cycles).Phenomic lag in the other direction, from pawn to wild type, varies from 0 to 2 cell cycles. The major cytoplasmic factor involved is the amount of wild-type material acquired from the mate during conjugation. Extensive cytoplasmic exchange often occurs during normal conjugation and can lead to change of phenotype as early as the first meiotic division. Phenotypic change due to gene expression in macronuclear anlagen brings about phenotypic change near the end of the first cell cycle in +/+ cells and about a cell cycle later in heterozygotes.


HortScience ◽  
1995 ◽  
Vol 30 (4) ◽  
pp. 809B-809
Author(s):  
Dennis J. Werner ◽  
Michael A. Creller

Inheritance of male sterility in peach [Prunus persica (L.) Batsch] Plant Introduction (PI) 240928 was investigated. Crosses of PI 240928 with five wild-type clones yielded all male-sterile offspring, indicating dominant gene action. Inheritance of the sweet kernel trait in peach was studied in F1 and F2 progeny of `Summer Beaut' nectarine (sweet kernel) × `Biscoe' peach (bitter kernel). All four F1 progeny were bitter. Segregation in an F2 of 80 progeny fit a ratio of 3 bitter: 1 sweet. We propose that the gene controlling the sweet kernel trait be designated sk. Sweet kernel (sk) was linked to nectarine (g) at a map distance of 17 cM. Evaluation of the peach PI collection showed that PI 129678 (`Stanwick' nectarine) and PI 34685 (`Quetta' nectarine) were the only clones with a sweet kernel. Crosses between `Davie II' and `Honeyglo' nectarine (dwdw) confirmed that the gene conferring the dwarf phenotype in progeny of `Davie II' is non-allelic to dw.


Genetics ◽  
1980 ◽  
Vol 94 (4) ◽  
pp. 933-950
Author(s):  
Dennis Nyberg

ABSTRACT The trichocysts of most wild stocks of Paramecium tetraurelia discharge en masse in response to picric acid. In most nonresponding wild stocks, the defective phenotype is simply determined by a single recessive gene difference from the standard wild type, stock 51. However, two wild stocks, 146 and 148, which are completely homozygous at all loci, eqress either a nondischarge, ND, or discharge, DI, phenotype. In stock 146, both ND and DI sublines generally reproduce true to type, but observed changes are highly biased. Changes from ND to DI occur more than ten times as often as changes from DI to ND. After conjugation between ND and DI cells, genomically identical exconjugant lines from the ND parent may be either ND or DI, while thme from the DI parent invariably remain D1.—Interstock crosses between stocks 146 and 51 indicate that stock 146 possesses a recessive gene, nd146, which, when hommygous in stock 51 background, produces a distinct nondischarge phenotype, KO. Crosses between stock 146 and KO phenotype nd146 homozygotes in stock 51 background demonstrate that stock 146 possesses a dominant gene, M-ndl46, which modifies the defect of nd146 homozygotes, resulting in either the ND or DI phenotype. The two loci, M-ndl46 and nd146, are linked and estimated to be 5.3 centiMorgans apart. Stock 148 has the same alleles as stock 146 at these loci.—Presumably M-nd146 is involved in the dual phenotypic states in stock 146, but M-ndl46 nd146 homozygotes backcrossed into stock 51 are invariably discharging. The possibility that the original ND state is independent of these genes is discussed and is regarded as unlikely. The phenotypic and genetic relationship discovered in these stocks should remind population biologists that phenotypic and genotypic variability do not always have a simple relationship. The nature and frequency of epistasis in the highly inbreeding P . teiraurelia are reviewed.


2005 ◽  
Vol 4 (10) ◽  
pp. 1613-1619 ◽  
Author(s):  
Atsushi Matsuda ◽  
James D. Forney

ABSTRACT In Paramecium tetraurelia, variable surface antigen loci show mutually exclusive expression which is controlled primarily at the transcriptional level. Clonally stable expression of a single antigen has attracted models involving self-regulation by their gene products. However, direct demonstration of self-feedback at the molecular level has been complicated due to the inability to separate the functional gene from its product as well as copy number effects associated with injected extrachromosomal DNA in the polygenomic somatic nucleus. In this study, we exploited several germ line termination and frameshift mutations in the A-51 surface antigen gene to analyze variable surface antigen expression. These mutant alleles have the same copy number as the wild-type allele and therefore eliminate possible copy number effects. The mutant alleles were not transcribed at 27°C, consistent with positive-feedback models for gene expression. However, further analysis showed that high temperatures (34°C) induced transcription of the mutant A genes even in the presence of a different antigen on the cell surface. Thus, transcription was temperature dependent. Unlike wild-type cells, transcription of the mutant A genes at high temperatures was not maintained after temperature shift back to 27°C in homozygous mutant cells. Importantly, transcription of the mutant allele was maintained at 27°C in heterozygous cells with one copy of the wild-type allele. These results indicate that expression of the wild-type gene is required to stabilize its own transcriptional state at 27°C.


HortScience ◽  
1998 ◽  
Vol 33 (3) ◽  
pp. 534b-534
Author(s):  
James D. McCreight

Yellowing of melon (Cucumis melo L.) incited by lettuce infectious yellows virus (LIYV) reduces yield and fruit quality of infected plants. LIYV is transmitted only by the sweetpotato whitefly (Bemisia tabaci Genn.). Two naturally infected field tests indicated several potential sources of resistance to LIYV. PI 124112 and `Snake Melon' had mild symptoms in both field tests whereas PI 313970 was asymptomatic in the test in which it was included. In greenhouse tests using controlled inoculation, PI 313970 was asymptomatic, had negative ELISA assays for LIYV, and was negative for LIYV in serial transfers to Chenopodium. `Top Mark' and `PMR 5' were symptomatic, had positive ELISA assays for LIYV, and were positive for LIYV in serial transfers to Chenopodium in these greenhouse tests. Limited data indicate that resistance in PI 313970 is conditioned by a single, dominant gene.


Biology ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 300
Author(s):  
Muhammad Miftahussurur ◽  
Dalla Doohan ◽  
Ari Fahrial Syam ◽  
Iswan Abbas Nusi ◽  
Phawinee Subsomwong ◽  
...  

CYP2C19 polymorphisms are important factors for proton pump inhibitor-based therapy. We examined the CYP2C19 genotypes and analyzed the distribution among ethnicities and clinical outcomes in Indonesia. We employed the polymerase chain reaction-restriction fragment length polymorphism method to determine the CYP2C19 genotypes and evaluated inflammation severity with the updated Sydney system. For CYP2C19*2, 46.4% were the homozygous wild-type allele, 14.5% were the homozygous mutated allele, and 39.2% were the heterozygous allele. For CYP2C19*3, 88.6% were the homozygous wild-type allele, 2.4% were the homozygous mutated allele, and 9.0% were the heterozygous allele. Overall, the prevalence of rapid, intermediate, and poor metabolizers in Indonesia was 38.5, 41.6, and 19.9%, respectively. In the poor metabolizer group, the frequency of allele *2 (78.8%) was higher than the frequency of allele *3 (21.2%). The Papuan had a significantly higher likelihood of possessing poor metabolizers than the Balinese (OR 11.0; P = 0.002). The prevalence of poor metabolizers was lower compared with the rapid and intermediate metabolizers among patients with gastritis and gastroesophageal reflux disease. Intermediate metabolizers had the highest prevalence, followed by rapid metabolizers and poor metabolizers. Dosage adjustment should therefore be considered when administering proton pump inhibitor-based therapy in Indonesia.


Genetics ◽  
2000 ◽  
Vol 155 (3) ◽  
pp. 1105-1117 ◽  
Author(s):  
W John Haynes ◽  
Kit-Yin Ling ◽  
Robin R Preston ◽  
Yoshiro Saimi ◽  
Ching Kung

Abstract Pawn mutants of Paramecium tetraurelia lack a depolarization-activated Ca2+ current and do not swim backward. Using the method of microinjection and sorting a genomic library, we have cloned a DNA fragment that complements pawn-B (pwB/pwB). The minimal complementing fragment is a 798-bp open reading frame (ORF) that restores the Ca2+ current and the backward swimming when expressed. This ORF contains a 29-bp intron and is transcribed and translated. The translated product has two putative transmembrane domains but no clear matches in current databases. Mutations in the available pwB alleles were found within this ORF. The d4-95 and d4-96 alleles are single base substitutions, while d4-662 (previously pawn-D) harbors a 44-bp insertion that matches an internal eliminated sequence (IES) found in the wild-type germline DNA except for a single C-to-T transition. Northern hybridizations and RT-PCR indicate that d4-662 transcripts are rapidly degraded or not produced. A second 155-bp IES in the wild-type germline ORF excises at two alternative sites spanning three asparagine codons. The pwB ORF appears to be separated from a 5′ neighboring ORF by only 36 bp. The close proximity of the two ORFs and the location of the pwB protein as indicated by GFP-fusion constructs are discussed.


Genetics ◽  
2002 ◽  
Vol 160 (1) ◽  
pp. 63-73
Author(s):  
Michael J McEachern ◽  
Dana Hager Underwood ◽  
Elizabeth H Blackburn

Abstract Telomerase adds telomeric DNA repeats to telomeric termini using a sequence within its RNA subunit as a template. We characterized two mutations in the Kluyveromyces lactis telomerase RNA gene (TER1) template. Each initially produced normally regulated telomeres. One mutation, ter1-AA, had a cryptic defect in length regulation that was apparent only if the mutant gene was transformed into a TER1 deletion strain to permit extensive replacement of basal wild-type repeats with mutant repeats. This mutant differs from previously studied delayed elongation mutants in a number of properties. The second mutation, TER1-Bcl, which generates a BclI restriction site in newly synthesized telomeric repeats, was indistinguishable from wild type in all phenotypes assayed: cell growth, telomere length, and in vivo telomerase fidelity. TER1-Bcl cells demonstrated that the outer halves of the telomeric repeat tracts turn over within a few hundred cell divisions, while the innermost few repeats typically resisted turnover for at least 3000 cell divisions. Similarly deep but incomplete turnover was also observed in two other TER1 template mutants with highly elongated telomeres. These results indicate that most DNA turnover in functionally normal telomeres is due to gradual replicative sequence loss and additions by telomerase but that there are other processes that also contribute to turnover.


1999 ◽  
Vol 380 (6) ◽  
Author(s):  
S.L. Nutt ◽  
M. Busslinger

AbstractIt is generally assumed that most mammalian genes are transcribed from both alleles. Hence, the diploid state of the genome offers the advantage that a loss-of-function mutation in one allele can be compensated for by the remaining wild-type allele of the same gene. Indeed, the vast majority of human disease syndromes and engineered mutations in the mouse genome are recessive, indicating that recessiveness is the ‘default’ state. However, a minority of genes are semi-dominant, as heterozygous loss-of-function mutation in these genes leads to phenotypic abnormalities. This condition, known as haploinsufficiency, has been described for five of the nine mammalian


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