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Background:
Environmental stress puts organisms at risk and requires specific stress-tailored responses to maximize
survival. Long-term exposure to stress necessitates a global reprogramming of the cellular activities at different
levels of gene expression.
Results:
Here, we use ribosome profiling and RNA sequencing to globally profile the adaptive response of
Arabidopsis thaliana
to prolonged heat stress. To adapt to long heat exposure, the expression of many genes is
modulated in a coordinated manner at a transcriptional and translational level. However, a significant group of
genes opposes this trend and shows mainly translational regulation. Different secondary structure elements are
likely candidates to play a role in regulating translation of those genes.
Conclusions:
Our data also uncover on how the subunit stoichiometry of multimeric protein complexes in plastids
is maintained upon heat exposure.
Background: Environmental stress puts organisms at risk and requires specific stress-tailored responses to maximize survival. Long-term exposure to stress necessitates a global reprogramming of the cellular activities at different levels of gene expression. Results: Here, we use ribosome profiling and RNA sequencing to globally profile the adaptive response of Arabidopsis thaliana to prolonged heat stress. To adapt to long heat exposure, the expression of many genes is modulated in a coordinated manner at a transcriptional and translational level. However, a significant group of genes opposes this trend and shows mainly translational regulation. Different secondary structure elements are likely candidates to play a role in regulating translation of those genes. Conclusions: Our data also uncover on how the subunit stoichiometry of multimeric protein complexes in plastids is maintained upon heat exposure.
Environmental stress is detrimental to cell viability and requires an adequate reprogramming of cellular activities to maximize cell survival. We present a global analysis of the response of Escherichia coli to acute heat and osmotic stress. We combine deep sequencing of total mRNA and ribosome-protected fragments to provide a genome-wide map of the stress response at transcriptional and translational levels. For each type of stress, we observe a unique subset of genes that shape the stress-specific response. Upon temperature upshift, mRNAs with reduced folding stability up-and downstream of the start codon, and thus with more accessible initiation regions, are translationally favoured. Conversely, osmotic upshift causes a global reduction of highly translated transcripts with high copy numbers, allowing reallocation of translation resources to not degraded and newly synthesized mRNAs.