Peter C. Breen
Harvard University
17 Papers
Peter C. Breen is an academic researcher from Harvard University. The author has contributed to research in topics: Biology & RNA interference. The author has an hindex of 9, co-authored 10 publications.
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Papers
Caenorhabditis elegans pathways that surveil and defend mitochondria
TL;DR: 45 C. elegans genes that are required to upregulate detoxification, pathogen-response and mitochondrial-repair pathways after inhibition of mitochondrial function by drug-induced or genetic disruption are identified from a genome-wide RNA interference screen.
MUT-16 promotes formation of perinuclear Mutator foci required for RNA silencing in the C. elegans germline
TL;DR: It is proposed that the mutator proteins and RRF-1 constitute an RNA processing compartment required for siRNA amplification and RNA silencing, and it is demonstrated that genes that yield high levels of siRNAs are disproportionally affected in mut-16 mutants compared with genes that fail to form at the nuclear periphery.
Protein Sequence Editing of SKN-1A/Nrf1 by Peptide:N-Glycanase Controls Proteasome Gene Expression.
TL;DR: An unexpected mechanism by which N-linked glycosylation regulates protein function and proteostasis is uncovered, which explains how ER-associated and cytosolic isoforms of SKN-1 perform distinct cytoprotective functions corresponding to those of mammalian Nrf1 and Nrf2.
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A microRNA program in the C. elegans hypodermis couples to intestinal mTORC2/PQM-1 signaling to modulate fat transport.
TL;DR: Results revealed that a non-cell-autonomous developmental input regulates intestinal fat metabolism by engaging mTORC2 signaling to promote the intertissue transport of fat reserves from the soma to the germline.
MUT-14 and SMUT-1 DEAD box RNA helicases have overlapping roles in germline RNAi and endogenous siRNA formation.
Carolyn M. Phillips,Brooke E Montgomery,Peter C. Breen,Elke F. Roovers,Young-Soo Rim,Toshiro K. Ohsumi,Martin A. Newman,Josien C. van Wolfswinkel,René F. Ketting,Gary Ruvkun,Taiowa A. Montgomery +10 more
TL;DR: It is shown that the DEAD box RNA helicase smut-1 functions redundantly in the mutator pathway with its paralog mut-14 during RNAi, pointing to a role for mut- 14 and smUT-1 in initiating siRNA amplification in germ cell Mutator foci, possibly through the recruitment or retention of target mRNAs.
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