Divergence in the ABA gene regulatory network underlies differential growth control.
The phytohormone abscisic acid (ABA) is a central regulator of acclimation to environmental stress; however, its contribution to differences in stress tolerance between species is unclear. To establish a comparative framework for understanding how stress hormone signalling pathways diverge across species, we studied the growth response of four Brassicaceae species to ABA treatment and generated transcriptomic and DNA affinity purification and sequencing datasets to construct a cross-species gene regulatory network (GRN) for ABA. Comparison of genes bound directly by ABA-responsive element binding factors suggests that cis-factors are most important for determining the target loci represented in the ABA GRN of a particular species. Using this GRN, we reveal how rewiring of growth hormone subnetworks contributes to stark differences in the response to ABA in the extremophyte Schrenkiella parvula. Our study provides a model for understanding how divergence in gene regulation can lead to species-specific physiological outcomes in response to hormonal cues.
View details for DOI 10.1038/s41477-022-01139-5
View details for PubMedID 35501452
Transcriptional acclimation and spatial differentiation characterize drought response by the ectomycorrhizal fungus Suillus pungens.
The New phytologist
Increasing temperature and decreasing precipitation has led to more frequent and extreme drought events in many regions throughout the world. In the western United States, multi-year drought events have led to widespread plant mortality and extreme wildfires (Asner et al. 2016, Pickrell and Pennisi 2020). Communities of ectomycorrhizal fungi (EMF) - root symbionts which play a critical role in forest health - are also thought to be threatened by these climatic changes (Fernandez et al. 2017, Steidinger et al. 2019). However, altered soil moisture conditions have complex direct and indirect effects on both fungi and ecosystem processes, such as nutrient availability (Schimel 2018), making it difficult to elucidate the primary drivers of community composition based on field observations or experiments (Pena and Polle 2014). As a result, efforts to identify the genes or traits involved in response to drought events are critical for accurate prediction of future EMF composition and function (Allison and Treseder 2008, Romero-Olivares et al. 2019). Despite this fact, we are not aware of any studies that have used gene expression analyses to measure the response of individual EMF to drought events or other climatic stressors.
View details for DOI 10.1111/nph.17816
View details for PubMedID 34668199
Prp8 impacts cryptic but not alternative splicing frequency
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
2019; 116 (6): 2193–99
Pre-mRNA splicing must occur with extremely high fidelity. Spliceosomes assemble onto pre-mRNA guided by specific sequences (5' splice site, 3' splice site, and branchpoint). When splice sites are mutated, as in many hereditary diseases, the spliceosome can aberrantly select nearby pseudo- or "cryptic" splice sites, often resulting in nonfunctional protein. How the spliceosome distinguishes authentic splice sites from cryptic splice sites is poorly understood. We performed a Caenorhabditis elegans genetic screen to find cellular factors that affect the frequency with which the spliceosome uses cryptic splice sites and identified two alleles in core spliceosome component Prp8 that alter cryptic splicing frequency. Subsequent complementary genetic and structural analyses in yeast implicate these alleles in the stability of the spliceosome's catalytic core. However, despite a clear effect on cryptic splicing, high-throughput mRNA sequencing of these prp-8 mutant C. elegans reveals that overall alternative splicing patterns are relatively unchanged. Our data suggest the spliceosome evolved intrinsic mechanisms to reduce the occurrence of cryptic splicing and that these mechanisms are distinct from those that impact alternative splicing.
View details for DOI 10.1073/pnas.1819020116
View details for Web of Science ID 000457731900061
View details for PubMedID 30674666