The Experts below are selected from a list of 303 Experts worldwide ranked by ideXlab platform
Abed Chaudhury - One of the best experts on this subject based on the ideXlab platform.
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plant genetics hothead healer and extragenomic information
Nature, 2005Co-Authors: Abed ChaudhuryAbstract:Arising from: S. J. Lolle, J. L. Victor, J. M. Young & R. E. Pruitt Nature 434, 505–509 (2005); see also communication from Ray ; Lolle et al. reply . Lolle et al. suggest that Non-Mendelian Inheritance in Arabidopsis thaliana might be attributable to an ancestral RNA-sequence cache1, whereby the RNA genome of previous generations causes a high rate of reversion of the plant's mutant hothead (hth) and erecta (er) genes. Here I describe a ‘distributed genome’ model that also explains their results, in which mutant hth DNA is restored by homologous sequences present in the genome itself. This model has implications for the generation of diversity without mating.
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Hothead healer and extragenomic information
Nature, 2005Co-Authors: Abed ChaudhuryAbstract:Arising from: S. J. Lolle, J. L. Victor, J. M. Young & R. E. Pruitt Nature 434 , 505–509 (2005); see also communication from Ray ; Lolle et al. reply . Lolle et al . suggest that Non-Mendelian Inheritance in Arabidopsis thaliana might be attributable to an ancestral RNA-sequence cache^ 1 , whereby the RNA genome of previous generations causes a high rate of reversion of the plant's mutant hothead ( hth ) and erecta ( er ) genes. Here I describe a ‘distributed genome’ model that also explains their results, in which mutant hth DNA is restored by homologous sequences present in the genome itself. This model has implications for the generation of diversity without mating.
Bernhard G. Herrmann - One of the best experts on this subject based on the ideXlab platform.
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Two isoforms of the RAC-specific guanine nucleotide exchange factor TIAM2 act oppositely on transmission ratio distortion by the mouse t-haplotype.
PLOS Genetics, 2019Co-Authors: Yves Charron, Bernhard G. Herrmann, Jürgen Willert, Barica Kusecek, Bettina Lipkowitz, Hermann BauerAbstract:Transmission ratio distortion (TRD) by the mouse t-haplotype, a variant region on chromosome 17, is a well-studied model of Non-Mendelian Inheritance. It is characterized by the high transmission ratio (up to 99%) of the t-haplotype from t/+ males to their offspring. TRD is achieved by the exquisite ability of the responder (Tcr) to trigger Non-Mendelian Inheritance of homologous chromosomes. Several distorters (Tcd1-Tcd4), which act cumulatively, together promote the high transmission ratio of Tcr and the t-haplotype. Molecularly, TRD is brought about by deregulation of Rho signaling pathways via the distorter products, which impair sperm motility, and the t-sperm specific rescue of sperm motility by the responder. The t-sperm thus can reach the egg cells faster than +-sperm and fertilize them. Previously we have shown that the responder function is accomplished by a dominant negative form of sperm motility kinase (SMOKTCR), while the distorter functions are accomplished by the Rho G protein regulators TAGAP, FGD2 and NME3 proposed to function in two oppositely acting pathways. Here we identify the RAC1-specific guanine nucleotide exchange factor TIAM2 as modifier of t-haplotype TRD. Tiam2 is expressed in two isoforms, the full-length (Tiam2l) and a short transcript (Tiam2s). Tiam2s expression from the t-allele is strongly increased compared to the wild-type allele. By transgenic approaches we show that Tiam2s enhances t-haplotype transmission, while Tiam2l has the opposite effect. Our data show that a single modifier locus can encode different gene products exerting opposite effects on a trait. They also suggest that the expression ratio of the isoforms determines if the outcome is an enhancing or a suppressive effect on the trait.
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The Nucleoside Diphosphate Kinase Gene Nme3 Acts as Quantitative Trait Locus Promoting Non-Mendelian Inheritance
PLOS Genetics, 2012Co-Authors: Hermann Bauer, Sabrina Schindler, Yves Charron, Jürgen Willert, Barica Kusecek, Bernhard G. HerrmannAbstract:The t-haplotype, a variant form of the t-complex region on mouse chromosome 17, acts as selfish genetic element and is transmitted at high frequencies (>95%) from heterozygous (t/+) males to their offspring. This phenotype is termed transmission ratio distortion (TRD) and is caused by the interaction of the t-complex responder (Tcr) with several quantitative trait loci (QTL), the t-complex distorters (Tcd1 to Tcd4), all located within the t-haplotype region. Current data suggest that the distorters collectively impair motility of all sperm derived from t/+ males; t-sperm is rescued by the responder, whereas +-sperm remains partially dysfunctional. Recently we have identified two distorters as regulators of RHO small G proteins. Here we show that the nucleoside diphosphate kinase gene Nme3 acts as a QTL on TRD. Reduction of the Nme3 dosage by gene targeting of the wild-type allele enhanced the transmission rate of the t-haplotype and phenocopied distorter function. Genetic and biochemical analysis showed that the t-allele of Nme3 harbors a mutation (P89S) that compromises enzymatic activity of the protein and genetically acts as a hypomorph. Transgenic overexpression of the Nme3 t-allele reduced t-haplotype transmission, proving it to be a distorter. We propose that the NME3 protein interacts with RHO signaling cascades to impair sperm motility through hyperactivation of SMOK, the wild-type form of the responder. This deleterious effect of the distorters is counter-balanced by the responder, SMOKTcr, a dominant-negative protein kinase exclusively expressed in t-sperm, thus permitting selfish behaviour and preferential transmission of the t-haplotype. In addition, the previously reported association of NME family members with RHO signaling in somatic cell motility and metastasis, in conjunction with our data involving RHO signaling in sperm motility, suggests a functional conservation between mechanisms for motility control in somatic cells and spermatozoa.
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Retention of gene products in syncytial spermatids promotes Non-Mendelian Inheritance as revealed by the t complex responder
Genes & Development, 2009Co-Authors: Nathalie Véron, Hermann Bauer, Andrea Y. Weiße, Gerhild Lüder, Martin Werber, Bernhard G. HerrmannAbstract:The t complex responder (Tcr) encoded by the mouse t haplotype is able to cause phenotypic differences between t and + sperm derived from t/+ males, leading to Non-Mendelian Inheritance. This capability of Tcr contradicts the concept of phenotypic equivalence proposed for sperm cells, which develop in a syncytium and actively share gene products. By analyzing a Tcr minigene in hemizygous transgenic mice, we show that Tcr gene products are post-meiotically expressed and are retained in the haploid sperm cells. The wild-type allele of Tcr, sperm motility kinase-1 (Smok1), behaves in the same manner, suggesting that Tcr/Smok reveal a common mechanism prone to evolve Non-Mendelian Inheritance in mammals.
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a protein kinase encoded by the t complex responder gene causes non mendelian Inheritance
Nature, 1999Co-Authors: Bernhard G. Herrmann, Birgit Koschorz, Karin Wertz, John K Mclaughlin, Andreas KispertAbstract:Males heterozygous for the t-haplotype form of mouse chromosome 17 preferentially transmit the t-chromosome to their progeny. Several distorter/sterility loci carried on the t-haplotype together impair flagellar function in all spermatozoa whereas the responder, Tcr, rescues t-sperm but not wild-type sperm. Thus, t-sperm have an advantage over wild-type sperm in fertilizing egg cells. We have isolated Tcr by positional cloning and show that it is a member of a novel protein kinase gene family, designated Smok, which is expressed late during spermiogenesis. Smok kinases are components of a signal cascade which may control sperm motility. Tcr has a reduced kinase activity, which may allow it to counterbalance a signalling impairment caused by the distorter/sterility loci. Tcr transgene constructs cause Non-Mendelian transmission of chromosomes on which they are carried, which leads to sex-ratio distortion when Tcr cosegregates with the Y chromosome.
Robert E Pruitt - One of the best experts on this subject based on the ideXlab platform.
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Plant genetics: Hothead healer and extragenomic information (reply)
Nature, 2005Co-Authors: Susan J. Lolle, Jennifer L. Victor, Jessica M. Young, Robert E PruittAbstract:Chaudhury 1 and Ray 2 propose alternative models to account for our observed pattern of Non-Mendelian Inheritance in the hothead (hth) mutant of Arabidopsis3.
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Genome-wide Non-Mendelian Inheritance of extra-genomic information in Arabidopsis
Nature, 2005Co-Authors: Susan J. Lolle, Jennifer L. Victor, Jessica M. Young, Robert E PruittAbstract:The principle of Inheritance first observed by Mendel is clear enough. Genetic information passes from parent to offspring in the DNA carried in the chromosomes found in every cell of the organism — and to a lesser extent in auxiliary genomes in organelles such as mitochondria and chloroplasts. But analysis of revertant hothead gene mutants in Arabidopsis thaliana suggests that these plants can inherit information not found in parental chromosomes, but identical to that of a grandparent or more distant forebear. This may involve template-directed restoration of ancestral DNA passed on in an RNA cache, like a web browser cache that delivers an old page. It will be intriguing to discover if this type of Inheritance is widespread. On the cover, a hothead mutant inflorescence (SEM by M. A. Webb). A fundamental tenet of classical mendelian genetics is that allelic information is stably inherited from one generation to the next, resulting in predictable segregation patterns of differing alleles1. Although several exceptions to this principle are known, all represent specialized cases that are mechanistically restricted to either a limited set of specific genes (for example mating type conversion in yeast2) or specific types of alleles (for example alleles containing transposons3 or repeated sequences4). Here we show that Arabidopsis plants homozygous for recessive mutant alleles of the organ fusion gene HOTHEAD5 (HTH) can inherit allele-specific DNA sequence information that was not present in the chromosomal genome of their parents but was present in previous generations. This previously undescribed process is shown to occur at all DNA sequence polymorphisms examined and therefore seems to be a general mechanism for extra-genomic Inheritance of DNA sequence information. We postulate that these genetic restoration events are the result of a template-directed process that makes use of an ancestral RNA-sequence cache.
K Mikami - One of the best experts on this subject based on the ideXlab platform.
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Non-Mendelian Inheritance ofMacronuclear Mutations IsGene Specific inParamecium tetraureliat
1994Co-Authors: K MikamiAbstract:Paramecium tetraurelia contains two typesofnuclei, a diploid germinal micronucleus anda large transcriptionally active macronucleus. Themacronuclear genome isformedfromthemicronuclear DNA during sexual reproduction. Previous studies haveshownthattheprocessing oftheA-type variable surface protein geneduring formation ofa new macronucleus isdependent on thepresenceoftheA geneintheold macronucleus.Itisnotclear ifthisisa general feature thatcontrols theformation oftheParamecium macronuclear genome or a unique feature oftheA locus. Usingmicronuclear transplantation, we have constructed a strain thathasa wild-type micronucleus buthasmacronuclear deletions oftheA-andB-type surface protein genes.Neither theA nor theB gene isincorporated intothenew macronucleus after sexual reproduction. Macronuclear transformation ofthis strain withtheB gene rescuestheB-gene deletion after formation ofthenextmacronucleus buthasno effect on theA deletion. Similarly, transformation withtheA geneshowsgene-specific rescueforAbutnotB.Theeffect oftheoldmacronucleus on theprocessing ofthenew macronucleus results ina pattern ofNon-Mendelian Inheritance ofbothmacronuclear deletions. Progeny from thewild-type exconjugant areallwild type,andprogenyfromtheA- B- exconjugant aremutant.Thefeatures ofthisA- B- Non-Mendelian mutantdemonstrate thattheregulation ofmacronuclear DNA processing is gene specific, andour results open thepossibility thatthistypeofregulation affects many regions ofthe Paramecium genome.
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Non-Mendelian Inheritance of macronuclear mutations is gene specific in Paramecium tetraurelia
Molecular and Cellular Biology, 1994Co-Authors: J M Scott, K Mikami, C L Leeck, James D. ForneyAbstract:Paramecium tetraurelia contains two types of nuclei, a diploid germinal micronucleus and a large transcriptionally active macronucleus. The macronuclear genome is formed from the micronuclear DNA during sexual reproduction. Previous studies have shown that the processing of the A-type variable surface protein gene during formation of a new macronucleus is dependent on the presence of the A gene in the old macronucleus. It is not clear if this is a general feature that controls the formation of the Paramecium macronuclear genome or a unique feature of the A locus. Using micronuclear transplantation, we have constructed a strain that has a wild-type micronucleus but has macronuclear deletions of the A- and B-type surface protein genes. Neither the A nor the B gene is incorporated into the new macronucleus after sexual reproduction. Macronuclear transformation of this strain with the B gene rescues the B-gene deletion after formation of the next macronucleus but has not effect on the A deletion. Similarly, transformation with the A gene shows gene-specific rescue for A but not B. The effect of the old macronucleus on the processing of the new macronucleus results in a pattern of Non-Mendelian Inheritance of both macronuclear deletions. Progeny from the wild-type exconjugant are all wild type, and progeny from the A- B- exconjugant are mutant. The features of this A- B- Non-Mendelian mutant demonstrate that the regulation of macronuclear DNA processing is gene specific, and our results open the possibility that this type of regulation affects many regions of the Paramecium genome.
Carole Charlier - One of the best experts on this subject based on the ideXlab platform.
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The callipyge mutation enhances bidirectional long-range DLK1-GTL2 intergenic transcription in cis.
Proceedings of the National Academy of Sciences of the United States of America, 2006Co-Authors: Haruko Takeda, Noelle Cockett, Samuel Hiard, Maria Smit, Xavier Tordoir, Florian Caiment, Michel Georges, Carole CharlierAbstract:The callipyge mutation (CLPG) is an A to G transition that affects a muscle-specific long-range control element located in the middle of the 90-kb DLK1-GTL2 intergenic (IG) region. It causes ectopic expression of a 327-kb cluster of imprinted genes in skeletal muscle, resulting in the callipyge muscular hypertrophy and its Non-Mendelian Inheritance pattern known as polar overdominance. We herein demonstrate that the CLPG mutation alters the muscular epigenotype of the DLK1-GTL2 IG region in cis, including hypomethylation, acquisition of novel DNase-I hypersentivite sites, and, most strikingly, strongly enhanced bidirectional, long-range IG transcription. The callipyge phenotype thus emerges as a unique model to study the functional significance of IG transcription, which recently has proven to be a widespread, yet elusive, feature of the mammalian genome.