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Biology subjects

Prasad, S. S.

Publications and source records attributed to Prasad, S. S..

2 recordsLinked to original sources

Multimodal Protein Retrieval via Joint Representation Learning from Sequences and Cryo-EM Density Maps

Aligning protein sequences with cryo-EM density maps remains challenging due to limited paired data, structural heterogeneity, varying map resolutions, and the presence of multiple conformational states. In this work, we propose a multimodal representation learning framework that learns a shared latent space between protein sequences and cryo-EM density maps for cross-modal retrieval. Our approach combines pretrained protein sequence embeddings with a volumetric cryo-EM encoder trained using self-supervised representation learning and transfer learning. The resulting model enables bidirectional retrieval between sequences and density maps while learning biologically meaningful structural representations. Experimental results demonstrate strong retrieval performance across both sequence-to-map and map-to-sequence tasks, achieving median retrieval ranks of 2--3 within a database of 3,275 cryo-EM maps. The learned embedding space shows a clear separation between matched and unmatched sequence--map pairs and remains robust across varying cryo-EM resolutions. Additionally, the model generalizes across species, successfully retrieving conserved mouse protein structures using human sequence embeddings. Our findings demonstrate that joint latent-space learning provides a promising direction for connecting protein sequences with cryo-EM structural representations, with potential applications in structural retrieval, protein annotation, and multimodal biological representation learning.

bioengineering↗

Gcn4 mediates SAM allocations and methylation balance between phospholipids and histones

Methionine availability alters the methylation status of various cellular molecules, and thereby controls metabolic state, via its metabolite S-adenosyl methionine (SAM). In yeast cells, supplementing excess methionine drives cell growth and proliferation, as well as phospholipid biogenesis. High methionine stabilizes the transcription factor Gcn4 (Atf4), which drives an anabolic transcription program to sustain high growth. Here, we investigated whether Gcn4 regulates the allocation of SAM towards distinct methylation outputs, during this methionine-dependent anabolic program. We find that methionine induced Gcn4 increases the expression of phospholipid methyltransferases during methionine supplementation. In{Delta} gcn4 cells, the expression of these methyltransferases significantly decreases, and results in reduced SAM allocations towards phospholipid methylation, alongside increased intracellular SAM, disrupting the balance in the SAM/SAH ratio in these cells. Excess SAM pools are re-allocated to histones, resulting in their hyper-methylation. Collectively, we uncover that Gcn4 modulates SAM allocations towards phospholipid methyltransferases, and the overall methyl allocation between phospholipids and histones. Our study reveals a novel role for Gcn4 in SAM dependent phospholipid biosynthesis in cells growing in methionine sufficiency.

cell biology↗