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Abstract High potassium (K) in the growth medium induces salinity stress in plants. However, the molecular mechanisms underlying plant responses to K-induced salt stress are virtually unknown. We examined Arabidopsis (Arabidopsis thaliana) and its extremophyte relative Schrenkiella parvula using a comparative multiomics approach to identify cellular processes affected by excess K and understand which deterministic regulatory pathways are active to avoid tissue damages while sustaining growth. Arabidopsis showed limited capacity to curb excess K accumulation and prevent nutrient depletion, contrasting to S. parvula which could limit excess K accumulation without restricting nutrient uptake. A targeted transcriptomic response in S. parvula promoted nitrogen uptake along with other key nutrients followed by uninterrupted N assimilation into primary metabolites during excess K-stress. This resulted in larger antioxidant and osmolyte pools and corresponded with sustained growth in S. parvula. Antithetically, Arabidopsis showed increased reactive oxygen species levels, reduced photosynthesis, and transcriptional responses indicative of a poor balance between stress signaling, subsequently leading to growth limitations. Our results indicate that the ability to regulate independent nutrient uptake and a coordinated transcriptomic response to avoid nonspecific stress signaling are two main deterministic steps toward building stress resilience to excess K+-induced salt stress. 

Autographa californica Multiple Nucleopolyhedrovirus (AcMNPV) is a baculovirus that causes systemic infections in many arthropod pests. The specific molecular processes underlying the biocidal activity of AcMNPV on its insect hosts are largely unknown. We describe the transcriptional responses in two major pests, Spodoptera frugiperda (fall armyworm) and Trichoplusia ni (cabbage looper), to determine the host–pathogen responses during systemic infection, concurrently with the viral response to the host. We assembled species-specific transcriptomes of the hemolymph to identify host transcriptional responses during systemic infection and assessed the viral transcript abundance in infected hemolymph from both species. We found transcriptional suppression of chitin metabolism and tracheal development in infected hosts. Synergistic transcriptional support was observed to suggest suppression of immune responses and induction of oxidative stress indicating disease progression in the host. The entire AcMNPV core genome was expressed in the infected host hemolymph with a proportional high abundance detected for viral transcripts associated with replication, structure, and movement. Interestingly, several of the host genes that were targeted by AcMNPV as revealed by our study are also targets of chemical insecticides currently used commercially to control arthropod pests. Our results reveal an extensive overlap between biological processes represented by transcriptional responses in both hosts, as well as convergence on highly abundant viral genes expressed in the two hosts, providing an overview of the host–pathogen transcriptomic landscape during systemic infection.