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Genetic and Developmental Implications for Trace Metal metabolism from Mutant and Inbred Strains of Animals
Published in Owen M. Rennert, Wai-Yee Chan, Metabolism of Trace Metals in Man, 2017
It is unlikely that any such degree of redundancy would occur or, if it did, would give rise to a viable genotype for the whole organism. Nevertheless, gene duplication is the presumed phylogenetic basis for acquisition of gene redundancy, as is commonly understood for the myoglobin and hemoglobin genes; numerous other redundant structural genes, as well as the two MT genes, may have originated also by gene duplication. Although much is known about MT, the genetic map location of the MT structural genes is still unknown. This may be due principally to the fact that there are no known or easily identifiable isothionein differences within MT-1 or MT-2; the determination of linkage maps requires such identifiable differences and the observance of recombinations with other known chromosomal markers.
Genomic Instability During Aging of Postmitotic Mammalian Cells
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
Many theories of aging consider DNA as a primary target for damage but stress the source of damage induction, such as oxygen radicals,29,30 while others point to possible sources of genetic instability such as transposon-mediated sequence rearrangements,31 chromosomal deletions of tandemly repeated genes,32 or selective loss of telomeric repetitive sequences.33 In contrast, other theories focus on the types of damage such as a single class of lesions, e.g., cross-linkages.34 In conjunction with underscoring the genome as a target of aging, some theories have featured genes and genetic mechanisms that counteract stochastic aging processes;2,3,35 these have included gene redundancy,36 DNA replication2,3,37,38 and repair machinery,2,3,39,40 and antioxidant defenses.41 The possibility that biological aging is genetically programmed has received some attention, too.9
The Parasite's Way of life
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2015
Eric S. Loker, Bruce V. Hofkin
Recent advances in genomics have greatly facilitated our ability to investigate the size, content, and organization of a parasite’s genome and to compare it to free-living forms. As new genomes become available, progress in our understanding of how genomes reflect lifestyle will no doubt accelerate. Certain trends are already well established. Prokaryotic intracellular parasites have among the smallest genomes of any cellular life form. Rickettsia prowazekii, for example, has approximately 830 protein-encoding genes, whereas Mycoplasma genitalium has only about 470. Escherichia coli, on the other hand, a fairly typical free-living species, has about 4200 protein-encoding genes. This trend toward genome reduction reflects a loss in biosynthetic and metabolic pathways as the parasite becomes increasingly dependent on the host. It has also been suggested that the reduced gene redundancy observed in many intracellular bacteria results from the relative stability of the host environment. In relatively unstable environments genetic redundancy provides the ability to adapt to changing conditions. In predictable environments this genetic flexibility is less of a concern. In other words, if it never rains, there is no need to carry an umbrella.
Virtual screening and zebrafish models in tandem, for drug discovery and development
Published in Expert Opinion on Drug Discovery, 2023
David Hernández-Silva, Francisca Alcaraz-Pérez, Horacio Pérez-Sánchez, Maria Luisa Cayuela
It is worth mentioning human genes that are associated with many zebrafish genes (the ‘one-human-to-many-zebrafish’ class), with an average of 2.28 zebrafish genes for each human gene [65]. This is because of an ancestor undergoing an additional round of whole-genome duplication. Gene redundancy, from an evolutionary point of view, helps an organism to survive when one copy of the homologs becomes nonfunctional or malfunctions or acquires a new function. However, it is undesirable for either the forward genetic approach to screen phenotypic mutants or reverse genetics to generate null alleles for target genes because the redundant genes might obscure the phenotypic drug screening or analysis.