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Philip C. J. Donoghue

Researcher at University of Bristol

Publications -  251
Citations -  17002

Philip C. J. Donoghue is an academic researcher from University of Bristol. The author has contributed to research in topics: Vertebrate & Molecular clock. The author has an hindex of 64, co-authored 231 publications receiving 14300 citations. Previous affiliations of Philip C. J. Donoghue include University of Birmingham & University of Leicester.

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Paleontological Evidence to Date the Tree of Life

TL;DR: This work provides "hard" minimum and "soft" maximum age constraints for 30 divergences among key genome model organisms; these should contribute to better understanding of the dating of the animal tree of life.
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Best practices for justifying fossil calibrations

TL;DR: A specimen-based protocol for selecting and documenting relevant fossils is presented and future directions for evaluating and utilizing phylogenetic and temporal data from the fossil record are discussed, to establish the best practices for justifying fossils used for the temporal calibration of molecular phylogenies.
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The timescale of early land plant evolution

TL;DR: A timescale for early land plant evolution that integrates over topological uncertainty by exploring the impact of competing hypotheses on bryophyte−tracheophyte relationships, among other variables, on divergence time estimation is established.
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Phylogenomic datasets provide both precision and accuracy in estimating the timescale of placental mammal phylogeny

TL;DR: A powerful Bayesian method is used to analyse 36 nuclear genomes and 274 mitochondrial genomes to reject a pre K–Pg model of placental ordinal diversification, and it is suggested other infamous instances of mismatch between molecular and palaeontological divergence time estimates will be resolved with this same approach.
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MicroRNAs and the advent of vertebrate morphological complexity

TL;DR: It is hypothesized that lying behind the origin of vertebrate complexity is the dramatic expansion of the noncoding RNA inventory including miRNAs, rather than an increase in the protein-encoding inventory caused by GDEs.