Fanconi's anaemia: correlation of genetic complementation group with psoralen/UVA response

1988 ◽  
Vol 78 (1) ◽  
pp. 51-54 ◽  
Author(s):  
Martin Digweed ◽  
Sabine Zakrzewski-L�dcke ◽  
Karl Sperling
Keyword(s):  
Complementation Group ◽  
Genetic Complementation

scholarly journals Microinjection of cytoplasm as a test of complementation in Paramecium.

1982 ◽  
Vol 92 (2) ◽  
pp. 559-564 ◽  
Author(s):  
N Haga ◽  
M Forte ◽  
Y Saimi ◽  
C Kung
Keyword(s):  
Action Potentials ◽  
Complementation Group ◽  
Genetic Complementation ◽  
Complementation Test ◽  
Paramecium Tetraurelia ◽  
Active Components ◽  
Cell Homogenate ◽  
A Cell ◽  
Complementation Groups ◽  
Favorable Conditions

Mutants in Paramecium tetraurelia, unable to generate action potentials, have been isolated as cells which show no backward swimming in response to ionic stimulation. These "pawn" mutants belong to at least three complementation groups designated pwA, pwB, and pwC. We have found that microinjection of cytoplasm from a wild-type donor into a pawn recipient of any of the three complementation groups restores the ability of the pawn to generate action potentials and hence swim backward. In addition, the cytoplasm from a pawn cannot restore a recipient of the same complementation group, but that from a pawn of a different group can. Electrophysiological analysis had demonstrated that the restoration of backward swimming is not due to a simple addition of ions but represents a profound change in the excitable membrane of the recipient pawn cells. Using known pawn mutants and those which had previously been unclassified, we have been able to establish a perfect concordance of genetic complementation and complementation by cytoplasmic transfer through microinjection. This method has been used to classify pawn mutants that are sterile or hard-to-mate and to examine the ability of cytoplasms from different species of ciliated protozoa to restore the ability to swim backward in the pawn mutants of P. tetraurelia. A cell homogenate has also been fractionated by centrifugation to further purify the active components. These results demonstrate that transfer of cytoplasm between cells by microinjection can be a valid and systematic method to classify mutants. This test is simpler to perform than the genetic complementation test and can be used under favorable conditions in mutants that are sterile and in cells of different species.

Early-lethal pulmonary form of Niemann-Pick type C disease belonging to a second, rare genetic complementation group

1998 ◽  
Vol 157 (1) ◽  
pp. 45-49 ◽  
Author(s):  
O. Schofer ◽  
B. Mischo ◽  
W. Püschel ◽  
K. Harzer ◽  
M. T. Vanier
Keyword(s):  
Complementation Group ◽  
Genetic Complementation ◽  
Type C ◽  
Niemann Pick

Sid patients bearing basaliomas in xeroderma pigmentosum complementation group F.

1990 ◽  
Vol 52 (2) ◽  
pp. 279-284 ◽  
Author(s):  
Seiji KONDO ◽  
Chizu MIYAMOTO ◽  
Chin-Huai KEONG ◽  
Yoshiaki SATOH ◽  
Yoshisada FUJIWARA ◽  
...  
Keyword(s):  
Xeroderma Pigmentosum ◽  
Complementation Group

Genetic complementation by cloned bacteriophage T4 late genes.

1981 ◽  
Vol 39 (1) ◽  
pp. 31-45 ◽  
Author(s):  
K A Jacobs ◽  
L M Albright ◽  
D K Shibata ◽  
E P Geiduschek
Keyword(s):  
Bacteriophage T4 ◽  
Genetic Complementation ◽  
Late Genes

scholarly journals MOLECULAR GENETIC ANALYSIS OF THE DILUTE-SHORT EAR (d-se) REGION OF THE MOUSE

Genetics ◽  
1986 ◽  
Vol 112 (2) ◽  
pp. 321-342
Author(s):  
Eugene M Rinchik ◽  
Liane B Russell ◽  
Neal G Copeland ◽  
Nancy A Jenkins
Keyword(s):  
Physical Map ◽  
Leukemia Virus ◽  
Molecular Genetic ◽  
Break Point ◽  
Virus Genome ◽  
Molecular Genetic Analysis ◽  
Chromosome 9 ◽  
Genetic Complementation ◽  
Induced Mutations ◽  
Radiation Induced

ABSTRACT Genes of the dilute-short ear (d-se) region of mouse chromosome 9 comprise an array of loci important to the normal development of the animal. Over 200 spontaneous, chemically induced and radiation-induced mutations at these loci have been identified, making it one of the most genetically well-characterized regions of the mouse. Molecular analysis of this region has recently become feasible by the identification of a dilute mutation that was induced by integration of an ecotropic murine leukemia virus genome. Several unique sequence cellular DNA probes flanking this provirus have now been identified and used to investigate the organization of wild-type chromosomes and chromosomes with radiation-induced d-se region mutations. As expected, several of these mutations are associated with deletions, and, in general, the molecular and genetic complementation maps of these mutants are concordant. Furthermore, a deletion break-point fusion fragment has been identified and has been used to orient the physical map of the d-se region with respect to the genetic complementation map. These experiments provide important initial steps for analyzing this developmentally important region at the molecular level, as well as for studying in detail how a diverse group of mutagens acts on the mammalian germline.

scholarly journals amontillado, the Drosophila Homolog of the Prohormone Processing Protease PC2, Is Required During Embryogenesis and Early Larval Development

Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 227-237 ◽  
Author(s):  
Lowell Y M Rayburn ◽  
Holly C Gooding ◽  
Semil P Choksi ◽  
Dhea Maloney ◽  
Ambrose R Kidd ◽  
...  
Keyword(s):  
Larval Development ◽  
Secretory Pathway ◽  
Larval Growth ◽  
Peptide Hormones ◽  
Complementation Group ◽  
Prohormone Processing ◽  
Complementation Groups ◽  
Regulated Secretory Pathway ◽  
Processing Protease ◽  
Larval Molt

Abstract Biosynthesis of most peptide hormones and neuropeptides requires proteolytic excision of the active peptide from inactive proprotein precursors, an activity carried out by subtilisin-like proprotein convertases (SPCs) in constitutive or regulated secretory pathways. The Drosophila amontillado (amon) gene encodes a homolog of the mammalian PC2 protein, an SPC that functions in the regulated secretory pathway in neuroendocrine tissues. We have identified amon mutants by isolating ethylmethanesulfonate (EMS)-induced lethal and visible mutations that define two complementation groups in the amon interval at 97D1 of the third chromosome. DNA sequencing identified the amon complementation group and the DNA sequence change for each of the nine amon alleles isolated. amon mutants display partial embryonic lethality, are defective in larval growth, and arrest during the first to second instar larval molt. Mutant larvae can be rescued by heat-shock-induced expression of the amon protein. Rescued larvae arrest at the subsequent larval molt, suggesting that amon is also required for the second to third instar larval molt. Our data indicate that the amon proprotein convertase is required during embryogenesis and larval development in Drosophila and support the hypothesis that AMON acts to proteolytically process peptide hormones that regulate hatching, larval growth, and larval ecdysis.

scholarly journals The tamas Gene, Identified as a Mutation That Disrupts Larval Behavior in Drosophila melanogaster, Codes for the Mitochondrial DNA Polymerase Catalytic Subunit (DNApol-γ125)

Genetics ◽  
1999 ◽  
Vol 153 (4) ◽  
pp. 1809-1824 ◽  
Author(s):  
Balaji Iyengar ◽  
John Roote ◽  
Ana Regina Campos
Keyword(s):  
Mitochondrial Dna ◽  
Drosophila Melanogaster ◽  
Mutant Strain ◽  
Dna Polymerase ◽  
Complementation Group ◽  
Behavioral Changes ◽  
Catalytic Subunit ◽  
Primary Deficit ◽  
Mitochondrial Dna Polymerase ◽  
Food Substrate

AbstractFrom a screen of pupal lethal lines of Drosophila melanogaster we identified a mutant strain that displayed a reproducible reduction in the larval response to light. Moreover, this mutant strain showed defects in the development of the adult visual system and failure to undergo behavioral changes characteristic of the wandering stage. The foraging third instar larvae remained in the food substrate for a prolonged period and died at or just before pupariation. Using a new assay for individual larval photobehavior we determined that the lack of response to light in these mutants was due to a primary deficit in locomotion. The mutation responsible for these phenotypes was mapped to the lethal complementation group l(2)34Dc, which we renamed tamas (translated from Sanskrit as “dark inertia”). Sequencing of mutant alleles demonstrated that tamas codes for the mitochondrial DNA polymerase catalytic subunit (DNApol-γ125).

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