Networks consist of systems’ components, referred to as ‘nodes’, and interactions between them, termed ‘edges’. The understanding of how networks function in the schema of an entire system is fueling the development of network based approaches. Such a framework is pertinent to evaluation of diverse biological networks co-expression, TF-target and protein-protein interactions. Network analysis has been a recent focus in biological sciences due to its ability to synthesize global visualizations of cellular processes and predict functions based on inferences from network properties. Understanding these topological features and deciphering the network architecture can provide insights into the identification of new community structures, unknown signaling pathways, and novel relationships between genes and their products. The work in my laboratory is focused on how macromolecular networks control biological processes and how environmental perturbations in such networks can explain diverse phenotypes.

Abiotic and biotic stresses can severely perturb endoplasmic reticulum (ER) function. The unfolded protein response (UPR) is a three-pronged signaling axis dedicated to preserving ER homeostasis. If these mechanisms of adaptation and survival are insufficient to recover the ER homeostasis, cells will initiate apoptosis.
My laboratory focuses on two main branches of UPR. GCN2 (general control nonderepressible 2) is a serine/threonine-protein kinase that acts as a global eukaryotic translational regulator. GCN2 mitigates cellular stresses by directly binding with uncharged tRNAs and phosphorylating its target, eukaryotic initiation factor 2 alpha (eIF2α). We demonstrate that GCN2 is involved in ABA signaling and stomatal immunity by affecting the pathogen-triggered stomatal closure and coronatine-mediated stomatal reopening.
Another UPR sensor, IRE1 (Inositol-requiring enzyme 1) directly cleaves bZIP60 (basic leucine zipper 60) mRNA in response to various environmental stresses, leading to the production of an active transcription factor that promotes the expression of multiple ER stress-responsive genes. We identified IRE1 signaling components that activate cellular pro-survival pathways, but under acute or chronic conditions can induce pro-death responses leading to apoptosis.