# Osmotic Stress Sensing and Signal Transduction in Arabidopsis > **NIH NIH R35** · UNIVERSITY OF CALIFORNIA, SAN DIEGO · 2024 · $395,000 ## Abstract PROJECT SUMMARY Hyperosmotic stress has been linked to several human diseases. Furthermore, drought-linked hyperosmotic stress is of major concern for threatening human nutrition and health. However, these osmotic/drought stress sensors and the early osmotic stress signal transduction mechanisms have remained largely unknown. Hyperosmotic stress triggers rapid intracellular Ca2+ transients in Arabidopsis. Moreover, we have recently discovered rapidly-activated Raf-kinases that are required for early hyperosmotic stress signal transduction in Arabidopsis. These early signal transduction mechanisms are required for resistance mechanisms, including downstream biosynthesis of the stress resistance hormone abscisic acid. Rapid osmotic stress responses in the highly developed Arabidopsis model organism provide an ideal system for dissection of a eukaryotic osmotic stress sensing and signal transduction machinery. The long-term objective of this research program is to achieve a molecular, cellular, mechanistic and quantitative understanding of osmotic stress sensing and signal transduction in the genetically tractable Arabidopsis model system. We will address the question of the unresolved osmotic stress sensor machinery and signal transduction cascade, through an innovative screen and new mutants we have isolated that greatly impair the rapid osmotic stress-induced Ca2+ transients. Moreover, downstream of hyperosmotic stress, we have recently found osmotic stress-triggered genome-wide chromatin remodeling that correlates with osmotic stress-induced transcriptome responses. The question of how osmotic stress signal transduction links to and mediates osmotic stress-induced genome reprogramming will be pursued. Furthermore, the question whether osmotic stress-induced chromatin remodeling primes the genome for future stress resistance will be investigated and underlying mechanisms will be determined. Another question of particular interest is how guard cells rapidly close stomata in response to low humidity (high vapor pressure difference), thereby reducing water loss. This elusive cellular low-humidity sensing and signal transduction pathway has been hypothesized to be related to osmotic stress sensing and signaling. We have recently discovered Raf-kinases, overlapping with the above-mentioned hyperosmotic stress-activated Raf- kinases, and a transmembrane receptor like pseudo kinase that are required for the rapid low humidity response in guard cells, providing a foothold for dissecting the underlying molecular and cellular signal transduction pathway. My laboratory applies diverse cellular signaling, genetic, genomic, biophysical and time-resolved imaging approaches to address fundamental questions in stress sensing and signaling. Results from this research will illuminate the elusive osmotic/drought and humidity sensing and signaling mechanisms and could lead to future strategies for improving food security for human health and nutrition. ## Key facts - **NIH application ID:** 10842151 - **Project number:** 1R35GM153381-01 - **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN DIEGO - **Principal Investigator:** JULIAN I SCHROEDER - **Activity code:** R35 (R01, R21, SBIR, etc.) - **Funding institute:** NIH - **Fiscal year:** 2024 - **Award amount:** $395,000 - **Award type:** 1 - **Project period:** 2024-06-01 → 2029-04-30 ## Primary source NIH RePORTER: https://reporter.nih.gov/project-details/10842151 ## Citation > US National Institutes of Health, RePORTER application 10842151, Osmotic Stress Sensing and Signal Transduction in Arabidopsis (1R35GM153381-01). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10842151. Licensed CC0. --- *[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*