bioRxiv Science⌕ Search

Biology subjects

Marty, T.

Publications and source records attributed to Marty, T..

2 recordsLinked to original sources

High-resolution dissection of concept acquisition in different families of protein language models

Protein language models have been increasingly successful on tasks ranging from fitness prediction to functional design, yet what biological knowledge they acquire and where it is encoded within their internal representations remain underexplored. Through a high-resolution layer-by-layer interpretability analysis of 8 models from the ESM2 and AMPLIFY families on 22 concepts from human proteome annotations, we found that these models encode concepts of increasing levels of complexity along their depth: basic physicochemical properties and linear motifs are best captured by early-layer embeddings, secondary structure from subsequent layers, and domain-level semantics from middle layers. Principal component projections of these embeddings showed that they separate biologically meaningful protein groupings, and molecular-biology-inspired interventions demonstrated that pLM embeddings can discriminate phosphomimic-active from inactive mutants. Perhaps surprisingly, we observed that pretraining data and compute had a greater impact on the linear emergence of biological concepts than scaling up parameters. By revealing where biological knowledge is captured in pLMs and which choices shape its emergence, our work offers insights to develop more robust, biologically grounded protein language models.

bioinformatics↗

Mutants of p53 sustain tumor growth under mechanical compression

ContextSolid tumors are subjected to mechanical stimuli arising from their growth in confined environments. Growth-induced pressure builds up in tumors such as pancreatic cancer and rises alongside the occurrence of genetic alterations during tumorigenesis. This study aims to understand the so far unknown relationship between genetic alterations and cancer cell behavior under compressive stress. ResultsUsing isogenic cell lines with engineered p53 mutations, we showed that the p53 background influences cell response to compression. Tumor growth under compression increased in cells harboring a mutated-truncated p53 form. This mutation blocked caspase 3 cleavage and promoted survival and growth through PI3K-AKT activation and dysregulation of c-FOS and FOSB transcription factors network. Mutated-truncated p53 cells displayed a unique behavior and heightened an activation state under compression. ConclusionMechanical compression and p53 mutations together drive tumor growth. p53 status could be a biomarker for predicting tumor adaptation to mechanical stress and efficiency of therapies targeting mechanosensitive pathways. TeaserMechanical compression and p53 mutations together enhance cancer cell survival and growth, driving solid tumor progression.

cancer biology↗