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Biomedical subjects

Jingting Yu

Publications and source records attributed to Jingting Yu.

2 recordsLinked to original sources

Drought recovery in plants triggers a cell-state-specific immune activation.

All organisms experience stress as an inevitable part of life, from single-celled microorganisms to complex multicellular beings. The ability to recover from stress is a fundamental trait that determines the overall resilience of an organism, yet stress recovery is understudied. To investigate how plants recover from drought, we examine a fine-scale time series of RNA sequencing starting 15 min after rehydration following moderate drought. We reveal that drought recovery is a rapid process involving the activation of thousands of recovery-specific genes. To capture these rapid recovery responses in different Arabidopsis thaliana (A. thaliana) leaf cell types, we perform a single-nucleus transcriptome analysis at the onset of drought recovery, identifying a cell type-specific transcriptional state developing independently across cell types. To further validate the cell-type specific transcriptional changes observed during drought recovery, we employ spatial transcriptomics using multiplexed error-robust fluorescence in situ hybridization (MERFISH), revealing anatomical localization of recovery-induced gene expression programs across Arabidopsis leaf tissues. Furthermore, we reveal a recovery-induced activation of the immune system that occurs autonomously, and which enhances pathogen resistance in vivo in A. thaliana, wild tomato (Solanum pennellii) and domesticated tomato (Solanum lycopersicum cv. M82). Since rehydration promotes microbial proliferation and thereby increases the risk of infection, the activation of drought recovery-induced immunity may be crucial for plant survival in natural environments. These findings indicate that drought recovery coincides with a preventive defense response, unraveling the complex regulatory mechanisms that facilitate stress recovery in different plant cell types.

Arabidopsis

Mathematical modeling suggests 14-3-3 proteins modulate RAF paradoxical activation.

RAF inhibitor "paradoxical activation" (PA) is a phenomenon where RAF kinase inhibitors increase RAF kinase signaling. Through mathematical modeling and experimental data analysis, we recently demonstrated that the combination of conformational autoinhibition (CA) with the disruption of CA by RAF inhibitors plays an important role in PA. 14-3-3 proteins are known to modulate RAF CA and RAF dimerization. We here extend our mathematical model to include both roles of 14-3-3 proteins, and we derive rigorous analytical expressions of RAF signal regulation as modulated by 14-3-3 proteins. We then use the model to investigate how 14-3-3 proteins may modulate PA. We mathematically show 14-3-3 protein stabilization of the autoinhibited form of RAF should potentiate PA, while 14-3-3 protein stabilization of the active RAF dimer should reduce PA. Our analysis suggests that the net-effect will often be a potentiation of PA, and that 14-3-3 proteins may be capable of inducing PA for RAF inhibitors that normally show little to no PA. We test model-based insights experimentally with two different approaches: forced increases in 14-3-3 expression (which we find amplifies PA) and evolved resistance assays (which suggest increased 14-3-3 expression may contribute to resistance to RAF inhibitors). Overall, this work supports a role for 14-3-3 in modulating RAF-inhibitor mediated paradoxical activation.

14-3-3 Proteins