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The emergence of highly adaptive or invasive bacterial clones is often explained by invoking the "epidemic" population structure in which a small number of successful clones dramatically increase their population size against the few background genotypes [8].
First, the frequency distribution of TCR clones is often used to quantify repertoire diversity.
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Mammalian clones are often extra-large, and pregnant mothers become dangerously swollen and frequently miscarry.
One of the expected dangers of cloning is that worn down telomeres will be inherited from the adult cells used in lieu of an egg or sperm cell, and indeed the telomeres of adult clones are often shorter than normal.
Under these experimental conditions, multiple clones were often induced in each testis.
Genetically-distinct malaria clones are often present in the same human blood meal so this sexual phase provides an opportunity for genetic recombination to occur between genetically-distinct malaria parasites, resulting in the generation of genetic diversity.
These clones are often vastly over-sampled due to their clinical importance and show strong clonality.
Nevertheless these clones were often sufficiently old to have accumulated somatic mutations for selected traits (fig skin color) and at neutral loci (microsatellite markers).
We have also observed that egg chambers containing trc, fry, or msn mutant follicle cell clones are often shorter and rounder than wild-type egg chambers.
The management of ex situ collections and the accurate identification of clones are often hampered by the lack of efficient markers.
Further, the loss of unstable or slowly growing clones which may have unique binding specificities often occurs during cloning and propagation and the strongly positive clones are often lost.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com