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Dawson, K.

Publications and source records attributed to Dawson, K..

3 recordsLinked to original sources

Random and non-random variation in flower color along an urban-rural gradient in the introduced mustard Hesperis matronalis

PremiseUrbanization can alter the interplay of stochastic genetic drift and natural selection but these effects will depend on the biology and history of a species. To explore the influences of drift and selection we investigated patterns of flower color variation among populations of the introduced ornamental mustard, Hesperis matronalis, along an urban-rural gradient in eastern Ontario Canada. MethodsWe surveyed 136 naturalized stands of H. matronalis over three generations, and for each stand estimated the diversity of the three color morphs (white, pink, purple), the number of reproductive plants, and the degree of urbanization based on night sky brightness. Key ResultsFlower color morph diversity increased with both stand size and urbanization which is consistent with effects of genetic drift during colonization combined with multiple introductions of this horticultural plant in urban areas. However, the frequency and fixation of the purple morph systematically increased towards the rural end of the gradient. Although lifetime seed production did not vary among morphs, pre-dispersal seed predation by a recently adventive weevil was higher in the purple morph, particularly in rural areas. Estimated seed production in the absence of predation suggests a previous fitness advantage for the purple and pink morphs in rural areas and for the white morph in urban areas. ConclusionsRandom variation in flower color diversity may be influenced by stochastic processes and colonization history, while systematic variation in color morph frequencies may reflect past fitness differences among morphs that have been recently erased by seed predation.

evolutionary biology↗

Clonal dynamics of haematopoiesis across the human lifespan

Age-related change in human haematopoiesis causes reduced regenerative capacity1, cytopenias2, immune dysfunction3 and increased risk of blood cancer. The cellular alterations that underpin the abruptness of this functional decline after the age of 70 years remain elusive. We sequenced 3579 genomes from single-cell-derived colonies of haematopoietic stem cell/multipotent progenitors (HSC/MPPs) across 10 haematologically normal subjects aged 0-81 years. HSC/MPPs accumulated 17 mutations/year after birth and lost 30bp/year of telomere length. Haematopoiesis in adults aged <65 was massively polyclonal, with high indices of clonal diversity and a stable population of 20,000-200,000 HSC/MPPs contributing evenly to blood production. In contrast, haematopoiesis in individuals aged >75 showed profoundly decreased clonal diversity. In each elderly subject, 30-60% of haematopoiesis was accounted for by 12-18 independent clones, each contributing 1-34% of blood production. Most clones had begun their expansion before age 40, but only 22% had known driver mutations. Genome-wide selection analysis estimated that 1/34 to 1/12 non-synonymous mutations were drivers, occurring at a constant rate throughout life, affecting a wider pool of genes than identified in blood cancers. Loss of Y chromosome conferred selective benefits on HSC/MPPs in males. Simulations from a simple model of haematopoiesis, with constant HSC population size and constant acquisition of driver mutations conferring moderate fitness benefits, entirely explained the abrupt change in clonal structure in the elderly. Rapidly decreasing clonal diversity is a universal feature of haematopoiesis in aged humans, underpinned by pervasive positive selection acting on many more genes than currently identified.

genomics↗

The mutational landscape of normal human endometrial epithelium

All normal somatic cells are thought to acquire mutations. However, characterisation of the patterns and consequences of somatic mutation in normal tissues is limited. Uterine endometrium is a dynamic tissue that undergoes cyclical shedding and reconstitution and is lined by a gland-forming epithelium. Whole genome sequencing of normal endometrial glands showed that most are clonal cell populations derived from a recent common ancestor with mutation burdens differing from other normal cell types and manyfold lower than endometrial cancers. Mutational signatures found ubiquitously account for most mutations. Many, in some women potentially all, endometrial glands are colonised by cell clones carrying driver mutations in cancer genes, often with multiple drivers. Total and driver mutation burdens increase with age but are also influenced by other factors including body mass index and parity. Clones with drivers often originate during early decades of life. The somatic mutational landscapes of normal cells differ between cell types and are revealing the procession of neoplastic change leading to cancer.

cancer biology↗