Jose M. Eirin-Lopez

Dr. Jose M. Eirin-Lopez

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Research Focus & Metrics

Academic Career Length

25Years (2002-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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31 May 2012 in Epigenetics & Chromatin
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Journal Article
Open access
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PTPaul B Talbert
Paul B Talbert
KAKami Ahmad
Kami Ahmad
GAGenevieve Almouzni
Genevieve Almouzni
Juan AusioJuan Ausio
Juan Ausio
FBFrédéric BERGER
Frédéric BERGER
SHSteven Henikoff
Steven Henikoff
Histone variants are non-allelic protein isoforms that play key roles in diversifying chromatin structure. The known number of such variants has greatly increased in recent years, but the lack of naming conventions for them has led to a variety of naming styles, multiple synonyms and misleading homographs that obscure variant relationships and complicate database searches. We propose here a unified nomenclature for variants of all five classes of histones that uses consistent but flexible naming conventions to produce names that are informative and readily searchable. The nomenclature builds on historical usage and incorporates phylogenetic relationships, which are strong predictors of structure and function. A key feature is the consistent use of punctuation to represent phylogenetic divergence, making explicit the relationships among variant subtypes that have previously been implicit or unclear. We recommend that by default new histone variants be named with organism-specific paralog-number suffixes that lack phylogenetic implication, while letter suffixes be reserved for structurally distinct clades of variants. For clarity and searchability, we encourage the use of descriptors that are separate from the phylogeny-based variant name to indicate developmental and other properties of variants that may be independent of structure.

3 January 2019 in Annual Review of Marine Science
Verified
Journal Article
Closed access
Jose M. Eirin-LopezJose M. Eirin-Lopez
Jose M. Eirin-Lopez
HPHollie Putnam
Hollie Putnam
Marine organisms’ persistence hinges on the capacity for acclimatization and adaptation to the myriad of interacting environmental stressors associated with global climate change. In this context, epigenetics—mechanisms that facilitate phenotypic variation through genotype–environment interactions—are of great interest ecologically and evolutionarily. Our comprehensive review of marine environmental epigenetics guides our recommendations of four key areas for future research: the dynamics of wash-in and wash-out of epigenetic effects, the mechanistic understanding of the interplay of different epigenetic marks and the interaction with the microbiome, the capacity for and mechanisms of transgenerational epigenetic inheritance, and the evolutionary implications of the interaction of genetic and epigenetic features. Emerging insights in marine environmental epigenetics can be applied to critical issues such as aquaculture, biomonitoring, and biological invasions, thereby improving our ability to explain and predict the responses of marine taxa to global climate change.

22 December 2006 in BioEssays
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Journal Article
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LFLindsay J. Frehlick
Lindsay J. Frehlick
Jose M. Eirin-LopezJose M. Eirin-Lopez
Jose M. Eirin-Lopez
Juan AusioJuan Ausio
Juan Ausio

1 November 2021 in Trends in Ecology & Evolution
Verified
Journal Article
Closed access
SHSerena Hackerott
Serena Hackerott
HMHarmony A. Martell
Harmony A. Martell
Jose M. Eirin-LopezJose M. Eirin-Lopez
Jose M. Eirin-Lopez

25 June 2012
Verified
Book Chapter
Closed access
Jose M. Eirin-LopezJose M. Eirin-Lopez
Jose M. Eirin-Lopez
LRLaureana Rebordinos
Laureana Rebordinos
ARA.P. Rooney
A.P. Rooney
JRJ. Rozas
J. Rozas
For quite some time, scientists have wondered how multigene families come into existence. Over the last several decades, a number of genomic and evolutionary mechanisms have been discovered that shape the evolution, structure and organization of multigene families. While gene duplication represents the core process, other phenomena such as pseudogene formation, gene loss, recombination and natural selection have been found to act in varying degrees to shape the evolution of gene families. How these forces influence the fate of gene duplicates has ultimately led molecular evolutionary biologists to ask the question: How and why do some duplicates gain new functions, whereas others deteriorate into pseudogenes or even get deleted from the genome? What ultimately lies at the heart of this question is the desire to understand how multigene families originate and diversify. The birth-and-death model of multigene family evolution provides a framework to answer this question. However, the growing availability of molecular data has revealed a much more complex scenario in which the birth-and-death process interacts with different mechanisms, leading to evolutionary novelty that can be exploited by a species as means for adaptation to various selective challenges. Here we provide an up-to-date review into the role of the birth-and-death model and the relevance of its interaction with forces such as genomic drift, selection and concerted evolution in generating and driving the evolution of different archetypal multigene families. We discuss the scientific evidence supporting the notion of birth-and-death as the major mechanism guiding the long-term evolution of multigene families.

14 December 2009 in BMC Biology
Verified
Journal Article
Open access
PDF file
DDDeanna Dryhurst
Deanna Dryhurst
TIToyotaka Ishibashi
Toyotaka Ishibashi
KRKristie L Rose
Kristie L Rose
Jose M. Eirin-LopezJose M. Eirin-Lopez
Jose M. Eirin-Lopez
DMDarin McDonald
Darin McDonald
Juan AusioJuan Ausio
Juan Ausio
Background: Within chromatin, the histone variant H2A.Z plays a role in many diverse nuclear processes including transcription, preventing the spread of heterochromatin and epigenetic transcriptional memory. The molecular mechanisms of how H2A.Z mediates its effects are not entirely understood. However, it is now known that H2A.Z has two protein isoforms in vertebrates, H2A.Z-1 and H2A.Z-2, which are encoded by separate genes and differ by 3 amino acid residues. Results: We report that H2A.Z-1 and H2A.Z-2 are expressed across a wide range of human tissues, they are both acetylated at lysine residues within the N-terminal region and they exhibit similar, but nonidentical, distributions within chromatin. Our results suggest that H2A.Z-2 preferentially associates with H3 trimethylated at lysine 4 compared to H2A.Z-1. The phylogenetic analysis of the promoter regions of H2A.Z-1 and H2A.Z-2 indicate that they have evolved separately during vertebrate evolution. Conclusions: Our biochemical, gene expression, and phylogenetic data suggest that the H2A.Z-1 and H2A.Z-2 variants function similarly yet they may have acquired a degree of functional independence.