Regulatory architecture tunes gene expression noise in the plant heat shock response
- 1Sainsbury Laboratory, University of Cambridge
Abstract
Cells within the same tissue can respond differently to the same stress, yet how gene regulatory networks generate and control this variability remains unclear. Here, we show that cell-to-cell variation in the Arabidopsis heat shock response is coordinated across the heat shock regulon and that the distribution of responses is tuned by the underlying regulatory network. Imaging of an HSP70 promoter reporter revealed basal activity in a subset of root cells and heterogeneous induction after heat shock, with some cells remaining near pre-stress expression levels. Dual reporters showed strong coordination between independently integrated HSP70 reporter loci, consistent with substantial shared upstream regulatory variation. Single-nucleus RNA sequencing confirmed heterogeneous but coordinated activation of heat shock genes across root cell types. Stronger heat shock states at both ambient and heat stress temperatures were associated with a recurrent thermoprotective programme across root cell populations, whereas weak responders after heat shock were associated with distinct cell-type specific transcriptional programmes, including defence- and jasmonate-associated states in some root cell types. Stochastic modelling suggested that HSFA2-dependent amplification could broaden the distribution of HSP70 expression across cells. Consistent with this prediction, experiments showed that loss of HSFA2 reduced HSP70 induction and lowered cell-to-cell variability after controlling for differences in mean expression. Together, these results show that the plant heat shock network controls both the magnitude and distribution of stress-responsive gene expression across cells.
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BibTeX
@misc{goswami2026regulatory,
title = {{Regulatory architecture tunes gene expression noise in the plant heat shock response}},
author = {R. Goswami and D. Cano Ramirez and K. Abley and M. Afsharinafar and C. Reynolds and J. Zeng and M. , Bhattarai and F. J. Zhang and S. Cortijo and A. Hall and E. S. Colizzi and J. C. W. Locke},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.22.760979},
url = {https://www.biorxiv.org/content/10.64898/2026.10.22.760979v1},
note = {CC BY-ND},
}
RIS
TY - UNPB
TI - Regulatory architecture tunes gene expression noise in the plant heat shock response
AU - R. Goswami
AU - D. Cano Ramirez
AU - K. Abley
AU - M. Afsharinafar
AU - C. Reynolds
AU - J. Zeng
AU - M. , Bhattarai
AU - F. J. Zhang
AU - S. Cortijo
AU - A. Hall
AU - E. S. Colizzi
AU - J. C. W. Locke
PY - 2026
DA - 2026/10/22
PB - bioRxiv
DO - 10.64898/2026.10.22.760979
UR - https://www.biorxiv.org/content/10.64898/2026.10.22.760979v1
AB - Cells within the same tissue can respond differently to the same stress, yet how gene regulatory networks generate and control this variability remains unclear. Here, we show that cell-to-cell variation in the Arabidopsis heat shock response is coordinated across the heat shock regulon and that the distribution of responses is tuned by the underlying regulatory network. Imaging of an HSP70 promoter reporter revealed basal activity in a subset of root cells and heterogeneous induction after heat shock, with some cells remaining near pre-stress expression levels. Dual reporters showed strong coordination between independently integrated HSP70 reporter loci, consistent with substantial shared upstream regulatory variation. Single-nucleus RNA sequencing confirmed heterogeneous but coordinated activation of heat shock genes across root cell types. Stronger heat shock states at both ambient and heat stress temperatures were associated with a recurrent thermoprotective programme across root cell populations, whereas weak responders after heat shock were associated with distinct cell-type specific transcriptional programmes, including defence- and jasmonate-associated states in some root cell types. Stochastic modelling suggested that HSFA2-dependent amplification could broaden the distribution of HSP70 expression across cells. Consistent with this prediction, experiments showed that loss of HSFA2 reduced HSP70 induction and lowered cell-to-cell variability after controlling for differences in mean expression. Together, these results show that the plant heat shock network controls both the magnitude and distribution of stress-responsive gene expression across cells.
ER -