Inference of evolutionary jumps in large phylogenies using Lévy processes

Although it is now widely accepted that the rate of phenotypic evolution may not necessarily be constant across large phylogenies, the frequency and phylogenetic position of periods of rapid evolution remain unclear. In his highly influential view of evolution, G. G. Simpson supposed that such evolutionary jumps occur when organisms transition into so-called new adaptive zones, for instance after dispersal into a new geographic area, after rapid climatic changes, or following the appearance of an evolutionary novelty. Only recently, large, accurate and well calibrated phylogenies have become available that allow testing this hypothesis directly, yet inferring evolutionary jumps remains computationally very challenging. Here, we develop a computationally highly efficient algorithm to accurately infer the rate and strength of evolutionary jumps as well as their phylogenetic location. Following previous work we model evolutionary jumps as a compound process, but introduce a novel approach to sample jump configurations that does not require matrix inversions and thus naturally scales to large trees. We then make use of this development to infer evolutionary jumps in Anolis lizards and Loriinii parrots where we find strong signal for such jumps at the basis of clades that transitioned into new adaptive zones, just as postulated by Simpson’s hypothesis

MOESM8 of Mechanistic differences between HIV-1 and SIV nucleocapsid proteins and cross-species HIV-1 genomic RNA recognition

Additional file 8: Fig. S7. SAXS data obtained for SIV Psi-∆DIS RNA (146 nt) and comparison to HIV-1 Psi-∆DIS (105 nt). a Plot of intensity versus momentum transfer for SIV Psi-∆DIS RNA. The open circles indicate every fifth data point from the experimental SAXS curve and the black line represents the back-calculated scattering curve of the ab initio envelope. The χ2 fit between the experimental and back-calculated ab initio envelope scattering curves is reported. b Comparison of the SIV Psi-∆DIS and HIV-1 Psi-∆DIS envelopes showing the confirmed SL structures of the RNAs [28]. The two envelopes were superimposed using the SUPCOMB program [113] and the NSD value for the comparison is indicated

Enrollment, allocation, and follow-up for trial subjects.

<p>The outcomes of the 41 screened subjects are described in the flow diagram.</p

Changes in immunologic, virologic, and cardiovascular parameters during 12 weeks after treatment crossover.

<p>Changes in immunologic, virologic, and cardiovascular parameters during 12 weeks after treatment crossover.</p

Changes in T cell activation and soluble markers aggregating the 12 weeks on mesalamine.

<p>Changes in T cell activation and soluble markers aggregating the 12 weeks on mesalamine.</p

Baseline Characteristics.

<p>ART, antiretroviral therapy; NRTI, nucleoside reverse transcriptase inhibitors; NNRTI, non-nucleoside reverse transcriptase inhibitors; PI, protease inhibitor; INSTI, integrase strand transfer inhibitor; AST, aspartate transaminase; ALT, alanine transaminase.</p><p>Baseline Characteristics.</p

Changes in immunologic, virologic, and cardiovascular parameters during the first 12 weeks of study.

<p>FMD, flow-mediated vasodilation of the brachial artery; K:T, kynurenine:tryptophan; VTI, velocity time integral.</p>a<p>There were 15 and 11 consented to mucosal biopsies in the placebo arm and mesalamine arm, respectively, but one in each arm did not contribute a second time point.</p>b<p>Total HIV RNA and DNA level from whole GALT biopsies were based on cell equivalents normalized by GAPDH and TERT copy number, respectively.</p><p>Changes in immunologic, virologic, and cardiovascular parameters during the first 12 weeks of study.</p