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Sebastian, L.

Publications and source records attributed to Sebastian, L..

3 recordsLinked to original sources

Optimization of the NFκB-DNA ensemble leads to high affinity binding of partial consensus sites

Our ability to respond to a myriad of external stressors is dependent on the activity of specific transcription factors that precisely regulate gene expression. While some transcription factors have high specificity for their consensus DNA binding site, others such as NF{kappa}B (RelA/p50) readily bind to partial and nonconsensus sites. In fact, ChIP-Seq data shows that nearly half of the DNA-bound RelA occupies sequences that do not match the consensus. Here we explore how NF{kappa}B (RelA/p50) binds to alternative sequences that differ subtly from the consensus. The two subunits of the NF{kappa}B heterodimer, RelA and p50, form an extensive pocket where DNA binding is mediated by both base-specific contacts and nonspecific interactions with the DNA backbone. RelA and p50 each form sequence-specific contacts with DNA at different 4-nucleotide sequences separated by two nucleotides, together forming a 10-base pair consensus binding sequence. Partial consensus sequences, known as half-sites, match the consensus sequence at only one of these two 4-nucleotide interaction sites. Here, using hydrogen deuterium exchange mass spectrometry (HDX-MS) and molecular dynamics (MD) simulations to investigate protein structural dynamics, we observe that rearranging nucleotides at the RelA-interacting end of a consensus DNA sequence to form a half-site induces dynamic structural changes through both subunits of RelA/p50. MD simulations reveal a shift in the position of DNA within the RelA/p50 binding pocket that allows optimal interaction with the half-site sequence. Our results demonstrate how RelA/p50 fine-tunes its interactions to achieve high-affinity binding with multiple different target DNA sequences.

biochemistry↗

Ergothioneine boosts mitochondrial respiration and exercise performance via direct activation of MPST

Ergothioneine (EGT) is a diet-derived, atypical amino acid that accumulates to high levels in human tissues. Reduced EGT levels have been linked to age-related disorders, including neurodegenerative and cardiovascular diseases, while EGT supplementation is protective in a broad range of disease and aging models in mice. Despite these promising data, the direct and physiologically relevant molecular target of EGT has remained elusive. Here we use a systematic approach to identify how mitochondria remodel their metabolome in response to exercise training. From this data, we find that EGT accumulates in muscle mitochondria upon exercise training. Proteome-wide thermal stability studies identify 3-mercaptopyruvate sulfurtransferase (MPST) as a direct molecular target of EGT; EGT binds to and activates MPST, thereby boosting mitochondrial respiration and exercise training performance in mice. Together, these data identify the first physiologically relevant EGT target and establish the EGT-MPST axis as a molecular mechanism for regulating mitochondrial function and exercise performance.

molecular biology↗

Oncogenic context shapes the fitness landscape of tumor suppression

Tumors acquire alterations in oncogenes and tumor suppressor genes in an adaptive walk through the fitness landscape of tumorigenesis. However, the features of this landscape remain poorly understood and cannot be revealed by human cancer genotyping alone. Here, we use a multiplexed, autochthonous mouse platform to model and quantify the initiation and growth of more than one hundred genotypes of lung tumors across four oncogenic contexts: KRAS G12D, KRAS G12C, BRAF V600E, and EGFR L858R. The resulting fitness landscape is rugged (the effect of tumor suppressor inactivation often switches between beneficial and deleterious depending on the oncogenic context), shows no evidence of diminishing-returns epistasis within variants of the same oncogene, and is inconsistent with expectations of a simple linear signaling relationship among these three oncogenes. Our findings suggest that tumor suppressor effects are strongly context-specific, which limits the set of evolutionary paths that can be taken through the fitness landscape.

cancer biology↗