ArticleBMC evolutionary biology2014
An evolutionary ratchet leading to loss of elongation factors in eukaryotes.
Article in BMC evolutionary biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- The geneFrontiers in microbiology · 2024Article
- Codon usage bias analysis of genes linked with esophagus cancer.Bioinformation · 2021Article
- ABCF ATPases Involved in Protein Synthesis, Ribosome Assembly and Antibiotic Resistance: Structural and Functional Diversification across the Tree of Life.Journal of molecular biology · 2019Article
- In Silico Structural Modeling and Analysis of Elongation Factor-1 Alpha and Elongation Factor-like Protein.ACS omega · 2019Article
- Evolutionarily conserved binding of translationally controlled tumor protein to eukaryotic elongation factor 1B.The Journal of biological chemistry · 2015Article
- The evolutionary and functional diversity of classical and lesser-known cytoplasmic and organellar translational GTPases across the tree of life.BMC genomics · 2015Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe GTPase eEF1A is the eukaryotic factor responsible for the essential, universal function of aminoacyl-tRNA delivery to the ribosome. Surprisingly, eEF1A is not universally present in eukaryotes, being replaced by the paralog EFL independently in multiple lineages. The driving force behind this unusually frequent replacement is poorly understood.
resultsThrough sequence searching of genomic and EST databases, we find a striking association of eEF1A replacement by EFL and loss of eEF1A's guanine exchange factor, eEF1Bα, suggesting that EFL is able to spontaneously recharge with GTP. Sequence conservation and homology modeling analyses indicate several sequence regions that may be responsible for EFL's lack of requirement for eEF1Bα.
conclusionsWe propose that the unusual pattern of eEF1A, eEF1Bα and EFL presence and absence can be explained by a ratchet-like process: if either eEF1A or eEF1Bα diverges beyond functionality in the presence of EFL, the system is unable to return to the ancestral, eEF1A:eEFBα-driven state.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.