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Benjamin Loppin

Researcher at Claude Bernard University Lyon 1

Publications -  40
Citations -  2600

Benjamin Loppin is an academic researcher from Claude Bernard University Lyon 1. The author has contributed to research in topics: Chromatin & Histone. The author has an hindex of 21, co-authored 35 publications receiving 2312 citations. Previous affiliations of Benjamin Loppin include Centre national de la recherche scientifique & University of Lyon.

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Removing symbiotic Wolbachia bacteria specifically inhibits oogenesis in a parasitic wasp

TL;DR: It is concluded that Wolbachia is necessary for oogenesis in these A. tabida strains, and this association would seem to be the first example of a transition from facultative to obligatory symbiosis in arthropod–Wolbachia associations.
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The histone H3.3 chaperone HIRA is essential for chromatin assembly in the male pronucleus

TL;DR: It is shown that ssm is a point mutation in the Hira gene, thus demonstrating that the histone chaperone protein HIRA is required for nucleosome assembly during sperm nucleus decondensation, and that nucleosomes containing H3.3, and not H3, are specifically assembled in paternal Drosophila chromatin before the first round of DNA replication.
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A unified phylogeny-based nomenclature for histone variants

Paul B. Talbert, +41 more
TL;DR: A unified nomenclature for variants of all five classes of histones is proposed that uses consistent but flexible naming conventions to produce names that are informative and readily searchable and incorporates phylogenetic relationships, which are strong predictors of structure and function.
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Parasitic inhibition of cell death facilitates symbiosis.

TL;DR: It is shown that Wolbachia influences programmed cell death processes in A. tabida, making its presence essential for the wasps' oocytes to mature, suggesting that parasite strategies, such as bacterial regulation of host apoptosis, can drive the evolution of host dependence, allowing for a swift transition from parasitism to mutualism.
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Wolbachia-mediated cytoplasmic incompatibility is associated with impaired histone deposition in the male pronucleus.

TL;DR: It is demonstrated that CI disrupts earlier interphase cell cycle events in the male pronucleus and proposed that these CI-induced interphase defects in de novo nucleosome assembly and replication are the cause of the observed mitotic condensation and segregation defects.