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Doan, L.

Publications and source records attributed to Doan, L..

3 recordsLinked to original sources

A Co-Evolutionary Multi-Objective Framework for Joint Topology and Parameter Discovery in Gene Regulatory Networks

Inferring gene regulatory networks (GRN) poses a complex discrete-continuous, multi-objective optimization problem that requires the simultaneous discovery of both network topology and kinetic parameters. Current methods are often limited because they address these two challenges separately. We propose a novel co-evolutionary multi-objective framework that evolves topology and parameter populations in tandem to optimize three competing objectives: dynamic fidelity, network simplicity, and robustness. This algorithm utilizes biologically-inspired operators and is grounded in theoretical results on Pareto optimality for mixed discrete-continuous spaces. In computational experiments on synthetic benchmarks, our approach showed superior performance, attaining the lowest mean squared error in three of four test cases against single-objective and topology-fixed methods. The framework successfully discovers multiple functionally equivalent network configurations, a finding that highlights the degeneracy inherent in biological systems and offers practical insights for synthetic biology, where function is often prioritized over precise structural accuracy.

systems biology↗

CryoEM and AI reveal a structure of SARS-CoV-2 Nsp2, a multifunctional protein involved in key host processes.

The SARS-CoV-2 protein Nsp2 has been implicated in a wide range of viral processes, but its exact functions, and the structural basis of those functions, remain unknown. Here, we report an atomic model for full-length Nsp2 obtained by combining cryo-electron microscopy with deep learning-based structure prediction from AlphaFold2. The resulting structure reveals a highly-conserved zinc ion-binding site, suggesting a role for Nsp2 in RNA binding. Mapping emerging mutations from variants of SARS-CoV-2 on the resulting structure shows potential host-Nsp2 interaction regions. Using structural analysis together with affinity tagged purification mass spectrometry experiments, we identify Nsp2 mutants that are unable to interact with the actin-nucleation-promoting WASH protein complex or with GIGYF2, an inhibitor of translation initiation and modulator of ribosome-associated quality control. Our work suggests a potential role of Nsp2 in linking viral transcription within the viral replication-transcription complexes (RTC) to the translation initiation of the viral message. Collectively, the structure reported here, combined with mutant interaction mapping, provides a foundation for functional studies of this evolutionary conserved coronavirus protein and may assist future drug design.

biophysics↗

Transient non-integrative nuclear reprogramming promotes multifaceted reversal of aging in human cells

Aging is characterized by a gradual loss of function occurring at the molecular, cellular, tissue and organismal levels1-3. At the chromatin level, aging is associated with the progressive accumulation of epigenetic errors that eventually lead to aberrant gene regulation, stem cell exhaustion, senescence, and deregulated cell/tissue homeostasis3. The technology of nuclear reprogramming to pluripotency, through over-expression of a small number of transcription factors, can revert both the age and the identity of any cell to that of an embryonic cell by driving epigenetic reprogramming2,4,5. Recent evidence has shown that transient transgenic reprogramming can ameliorate age-associated hallmarks and extend lifespan in progeroid mice6. However, it is unknown how this form of epigenetic rejuvenation would apply to physiologically aged cells and, importantly, how it might translate to human cells. Here we show that transient reprogramming, mediated by transient expression of mRNAs, promotes a rapid reversal of both cellular aging and of epigenetic clock in human fibroblasts and endothelial cells, reduces the inflammatory profile in human chondrocytes, and restores youthful regenerative response to aged, human muscle stem cells, in each case without abolishing cellular identity. Our method, that we named Epigenetic Reprogramming of Aging (ERA), paves the way to a novel, potentially translatable strategy for ex vivo cell rejuvenation treatment. In addition, ERA holds promise for in vivo tissue rejuvenation therapies to reverse the physiological manifestations of aging and the risk for the development of age-related diseases.

cell biology↗