Babesia bovis: Genome size, number of chromosomes and telomeric probe hybridisation

The number of different cell types (NCT) characterizing an organism is often used to quantify organismic complexity. This method results in the tautology that more complex organisms have a larger number of different kinds of cells, and that organisms with more different kinds of cells are more complex. This circular reasoning can be avoided (and simultaneously tested) when NCT is plotted against different measures of organismic information content (e.g., genome or proteome size). This approach is illustrated by plotting the NCT of representative diatoms, green and brown algae, land plants, invertebrates, and vertebrates against data for genome size (number of base-pairs), proteome size (number of amino acids), and proteome functional versatility (number of intrinsically disordered protein domains or residues). Statistical analyses of these data indicate that increases in NCT fail to keep pace with increases in genome size, but exceed a one-to-one scaling relationship with increasing proteome size and with increasing numbers of intrinsically disordered protein residues. We interpret these trends to indicate that comparatively small increases in proteome (and not genome size) are associated with disproportionate increases in NCT, and that proteins with intrinsically disordered domains enhance cell type diversity and thus contribute to the evolution of complex multicellularity.

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Evolution of linkage and genome expansion in protocells: The origin of chromosomes

PLoS Genetics ◽

10.1371/journal.pgen.1009155 ◽

2020 ◽

Vol 16 (10) ◽

pp. e1009155

Author(s):

András Szilágyi ◽

Viktor Péter Kovács ◽

Eörs Szathmáry ◽

Mauro Santos

Keyword(s):

Genome Size ◽

Marked Reduction ◽

Deleterious Mutations ◽

Remarkable Feature ◽

Intragenomic Conflict ◽

Size Number ◽

Added Benefit ◽

Chromosome Formation ◽

Selection Of ◽

Chromosome Level

Chromosomes are likely to have assembled from unlinked genes in early evolution. Genetic linkage reduces the assortment load and intragenomic conflict in reproducing protocell models to the extent that chromosomes can go to fixation even if chromosomes suffer from a replicative disadvantage, relative to unlinked genes, proportional to their length. Here we numerically show that chromosomes spread within protocells even if recurrent deleterious mutations affecting replicating genes (as ribozymes) are considered. Dosage effect selects for optimal genomic composition within protocells that carries over to the genic composition of emerging chromosomes. Lacking an accurate segregation mechanism, protocells continue to benefit from the stochastic corrector principle (group selection of early replicators), but now at the chromosome level. A remarkable feature of this process is the appearance of multigene families (in optimal genic proportions) on chromosomes. An added benefit of chromosome formation is an increase in the selectively maintainable genome size (number of different genes), primarily due to the marked reduction of the assortment load. The establishment of chromosomes is under strong positive selection in protocells harboring unlinked genes. The error threshold of replication is raised to higher genome size by linkage due to the fact that deleterious mutations affecting protocells metabolism (hence fitness) show antagonistic (diminishing return) epistasis. This result strengthens the established benefit conferred by chromosomes on protocells allowing for the fixation of highly specific and efficient enzymes.

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Within-population genome size variation is mediated by multiple genomic elements that segregate independently during meiosis

Genome Biology and Evolution ◽

10.1093/gbe/evz253 ◽

2019 ◽

Author(s):

Claus-Peter Stelzer ◽

Maria Pichler ◽

Peter Stadler ◽

Anita Hatheuer ◽

Simone Riss

Keyword(s):

Genome Size ◽

Size Variation ◽

Species Variation ◽

Evolutionary Potential ◽

Short Term ◽

Genome Size Variation ◽

Size Change ◽

Diploid Genome ◽

Individual Level ◽

Size Number

Abstract Within-species variation in genome size has been documented in many animals and plants. Despite its importance for understanding eukaryotic genome diversity, there is only sparse knowledge about how individual-level processes mediate genome size variation in populations. Here we study a natural population of the rotifer Brachionus asplanchnoidis whose members differ up to 1.9-fold in diploid genome size, but were still able to interbreed and produce viable offspring. We show that genome size is highly heritable and can be artificially selected up or down, but not below a certain basal diploid genome size for this species. Analyses of segregation patterns in haploid males reveal that large genomic elements (several megabases in size) provide the substrate of genome size variation. These elements, and their segregation patterns, explain the generation of new genome size variants, the short-term evolutionary potential of genome size change in populations, and some seemingly paradoxical patterns, like an increase in genome size variation among highly inbred lines. Our study suggests that a conceptual model involving only two variables, (1) a basal genome size of the population, and (2) a vector containing information on additional elements that may increase genome size in this population (size, number, and meiotic segregation behaviour), can effectively address most scenarios of short-term evolutionary change of genome size in a population.

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Within-population genome size variation is mediated by multiple genomic elements that segregate independently during meiosis

10.1101/623470 ◽

2019 ◽

Author(s):

Claus-Peter Stelzer ◽

Maria Pichler ◽

Peter Stadler ◽

Anita Hatheuer ◽

Simone Riss

Keyword(s):

Genome Size ◽

Size Variation ◽

Species Variation ◽

Genome Diversity ◽

Evolutionary Potential ◽

Short Term ◽

Genome Size Variation ◽

Size Change ◽

Individual Level ◽

Size Number

AbstractWithin-species variation in genome size has been documented in many animals and plants. Despite its importance for understanding eukaryotic genome diversity, there is only sparse knowledge about how individual-level processes mediate genome size variation in populations. Here we study a natural population of the rotifer Brachionus asplanchnoidis whose members differ up to 1.9-fold in genome size, but were still able to interbreed and produce viable offspring. We show that genome size is highly heritable and can be artificially selected up or down, but not beyond a minimum diploid genome size. Analyses of segregation patterns in haploid males reveal that large genomic elements (several megabases in size) provide the substrate of genome size variation. These elements, and their segregation patterns, explain the generation of new genome size variants, the short-term evolutionary potential of genome size change in populations, and some seemingly paradoxical patterns, like an increase in genome size variation among highly inbred lines. Our study suggests that a conceptual model involving only two variables, (1) a minimum genome size of the population, and (2) a vector containing information on additional elements that may increase genome size in this population (size, number, and meiotic segregation behaviour), can effectively address most scenarios of short-term evolutionary change of genome size in a population.

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Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100100378 ◽

1968 ◽

Vol 26 ◽

pp. 126-127

Author(s):

George Hug ◽

William K. Schubert

Keyword(s):

Heart Failure ◽

Biochemical Analysis ◽

Left Ventricular ◽

Size Number ◽

Internal Structures ◽

Left Ventricular Outflow ◽

Chest X Ray ◽

Myocardial Fibers ◽

Muscle Biopsies ◽

Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

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