Keyword search (4,163 papers available)

"Kachroo AH" Authored Publications:

Title Authors PubMed ID
1 A Humanized Yeast Model for Studying TRAPP Complex Mutations; Proof-of-Concept Using Variants from an Individual with a TRAPPC1-Associated Neurodevelopmental Syndrome Zykaj E; Abboud C; Asadi P; Warsame S; Almousa H; Milev MP; Greco BM; López-Sánchez M; Bratkovic D; Kachroo AH; Pérez-Jurado LA; Sacher M; 39273027
BIOLOGY
2 Erratum: Correction Notice: Single-step Precision Genome Editing in Yeast Using CRISPR-Cas9 Akhmetov A; Laurent JM; Gollihar J; Gardner EC; Garge RK; Ellington AD; Kachroo AH; Marcotte EM; 38161732
BIOLOGY
3 Species-specific protein-protein interactions govern the humanization of the 20S proteasome in yeast Sultana S; Abdullah M; Li J; Hochstrasser M; Kachroo AH; 37364278
BIOLOGY
4 Rapid, scalable, combinatorial genome engineering by marker-less enrichment and recombination of genetically engineered loci in yeast Abdullah M; Greco BM; Laurent JM; Garge RK; Boutz DR; Vandeloo M; Marcotte EM; Kachroo AH; 37323580
BIOLOGY
5 Humanized yeast to model human biology, disease and evolution Kachroo AH; Vandeloo M; Greco BM; Abdullah M; 35661208
BIOLOGY
6 Discovery of new vascular disrupting agents based on evolutionarily conserved drug action, pesticide resistance mutations, and humanized yeast Garge RK; Cha HJ; Lee C; Gollihar JD; Kachroo AH; Wallingford JB; Marcotte EM; 34849907
BIOLOGY
7 Humanization of yeast genes with multiple human orthologs reveals functional divergence between paralogs. Laurent JM, Garge RK, Teufel AI, Wilke CO, Kachroo AH, Marcotte EM 32421706
BIOLOGY
8 Single-step Precision Genome Editing in Yeast Using CRISPR-Cas9. Akhmetov A, Laurent JM, Gollihar J, Gardner EC, Garge RK, Ellington AD, Kachroo AH, Marcotte EM 29770349
BIOLOGY
9 The Many Nuanced Evolutionary Consequences of Duplicated Genes. Teufel AI, Johnson MM, Laurent JM, Kachroo AH, Marcotte EM, Wilke CO 30428072
BIOLOGY

 

Title:The Many Nuanced Evolutionary Consequences of Duplicated Genes.
Authors:Teufel AIJohnson MMLaurent JMKachroo AHMarcotte EMWilke CO
Link:https://www.ncbi.nlm.nih.gov/pubmed/30428072?dopt=Abstract
DOI:10.1093/molbev/msy210
Publication:Molecular biology and evolution
Keywords:
PMID:30428072 Category:Mol Biol Evol Date Added:2019-06-07
Dept Affiliation: BIOLOGY
1 Department of Integrative Biology, The University of Texas at Austin, Austin, TX.
2 Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX.
3 Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX.
4 Department of Biochemistry and Molecular Pharmacology, Institute for Systems Genetics, New York University Langone Health, New York, NY.
5 The Department of Biology, Centre for Applied Synthetic Biology, Concordia University, Montreal, QC, Canada.

Description:

The Many Nuanced Evolutionary Consequences of Duplicated Genes.

Mol Biol Evol. 2019 02 01;36(2):304-314

Authors: Teufel AI, Johnson MM, Laurent JM, Kachroo AH, Marcotte EM, Wilke CO

Abstract

Gene duplication is seen as a major source of structural and functional divergence in genome evolution. Under the conventional models of sub or neofunctionalization, functional changes arise in one of the duplicates after duplication. However, we suggest here that the presence of a duplicated gene can result in functional changes to its interacting partners. We explore this hypothesis by in silico evolution of a heterodimer when one member of the interacting pair is duplicated. We examine how a range of selection pressures and protein structures leads to differential patterns of evolutionary divergence. We find that a surprising number of distinct evolutionary trajectories can be observed even in a simple three member system. Further, we observe that selection to correct dosage imbalance can affect the evolution of the initial function in several unexpected ways. For example, if a duplicate is under selective pressure to avoid binding its original binding partner, this can lead to changes in the binding interface of a nonduplicated interacting partner to exclude the duplicate. Hence, independent of the fate of the duplicate, its presence can impact how the original function operates. Additionally, we introduce a conceptual framework to describe how interacting partners cope with dosage imbalance after duplication. Contextualizing our results within this framework reveals that the evolutionary path taken by a duplicate's interacting partners is highly stochastic in nature. Consequently, the fate of duplicate genes may not only be controlled by their own ability to accumulate mutations but also by how interacting partners cope with them.

PMID: 30428072 [PubMed - in process]





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