Research
Questions

I study how plants use calcium signaling to sense and respond to their environment, and how stress can disrupt these signals. I approach plant immunity through the lens of calcium signaling, using advanced biosensor imaging, molecular biology, biochemistry, and genetics to uncover how immune responses are regulated.

Whole-plant calcium imaging highlights signaling

diversity based on immune receptor activated during ETI.

Calcium signaling and bacterial growth at two temperatures. At elevated temperature (dotted line), the RPS4-dependent calcium signal fails to reach the immunity threshold, leading to ETI collapse and increased pathogen growth.

How Does Elevated Temperature Suppress Calcium Signaling During ETI?

Whole-plant calcium imaging shows that elevated temperature dampens the calcium influx normally triggered during effector-triggered immunity (ETI). This suppression correlates with a loss of resistance, but the underlying mechanisms are just now being resolved. Does temperature directly affect NLR receptor activity, and can we find mutations to confer temperature resilience for climate reilience immunity?

How is Immunity-Related Calcium Signaling Controlled Within Cells and Organelles?

Using advanced biosensor imaging, I track calcium dynamics at cellular and subcellular resolution during effector-triggered immunity (ETI). Several open question remain including 1) where does NLR-mediated calcium influx initiate within the cell, and 2) how are calcium signaling and immune outputs are coordinated between cells at the site of effector recognition and those in surrounding tissues?

Subcellular calcium signaling dynamics in an epidermal pavement cell during the onset of ETI

Temporal color coding tracks peak calcium levels

to illustrate spatiotemporal calcium signaling heterogeneity in the epidermis during ETI.

Plant-wide calcium signaling in response to a shift to high humidity.

Kymographic analysis highlights spatiotemporal patterns of calcium waves in the petioles in response to high humidity.

How Does Calcium Signaling Control Molecular and Physiological Responses to Humidity Change?

Climate-controlled imaging reveals that shifts in humidity trigger distinct calcium signatures, from rapid bursts to sustained waves. These signals are required for adaptive leaf movement, yet their mechanistic basis is still being resolved. How do cell wall integrity sensors and calcium channels integrate to mediate plant responses to fluctuating humidity?

Publications in Preparation

Opachaloemphan C*, Hilleary R*, Nomura K, He SY: FERONIA mediates plant adaptation to high humidity. (Submitted, target journal: PNAS). *co-first authors

Hilleary R, Grech-Baran M, Ahn HK, Oh E, Dong R, Chen Y, Liang M, Zhou P, He SY: Temperature-dependent suppression of Ca2+ signaling during effector-triggered immunity. (In preparation, target journal: PNAS).

Hilleary R, Sohrabi R, Withers S, McMillan H, Kim JH, He SY: Discovering Temperature-Resilient Nodes of Salicylic Acid Biosynthesis. (In preparation, target journal: Plant Direct).

How does pathogen signaling and metabolism change during infection?

Arabidopsis aca4/11 mutants lack two vacuolar calcium pumps, leading to spontaneous calcium waves and temperature-dependent lesions. As seedlings, these plants show heightened resistance to pathogens, yet as they mature they permit commensal microbes to overgrow, resulting in a dysbiotic community. This dual phenotype links disrupted calcium clearance not only to cell death and lesioning but also to the balance between protective immunity and microbial homeostasis.

aca4/11 mutants (left) and wildtype (right) grown at two different temperatures. aca4/11 plants exhibit spontaneous lesions, dwarfism, and autoimmunity at 23 °C.

Rosette leaf of an aca4/11 plant grown at 28 °C, then shifted to 23 °C immediately before imaging. Calcium wavefronts (segmented in green) can be seen. Areas with persistently elevated calcium precede lesion formation.