ArticleJournal of cell science2021
Activation of IRE1, PERK and salt-inducible kinases leads to Sec body formation in Drosophila S2 cells.
Article in Journal of cell science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- Endoplasmic reticulum and Golgi stress signaling-mediated regulation of protein secretion.Cellular & molecular biology letters · 2026Review
- Physiological implications of phase separation in vesicle organization and trafficking.BMC biology · 2026Review
- Article
- Article
- Stress-induced phase separation of ERES components into Sec bodies precedes ER exit inhibition in mammalian cells.Journal of cell science · 2022Article
- Identification of the stress granule transcriptome via RNA-editing in single cells andCell reports methods · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
The phase separation of the non-membrane bound Sec bodies occurs in Drosophila S2 cells by coalescence of components of the endoplasmic reticulum (ER) exit sites under the stress of amino acid starvation. Here, we address which signaling pathways cause Sec body formation and find that two pathways are critical. The first is the activation of the salt-inducible kinases (SIKs; SIK2 and SIK3) by Na+ stress, which, when it is strong, is sufficient. The second is activation of IRE1 and PERK (also known as PEK in flies) downstream of ER stress induced by the absence of amino acids, which needs to be combined with moderate salt stress to induce Sec body formation. SIK, and IRE1 and PERK activation appear to potentiate each other through the stimulation of the unfolded protein response, a key parameter in Sec body formation. This work shows the role of SIKs in phase transition and re-enforces the role of IRE1 and PERK as a metabolic sensor for the level of circulating amino acids and salt. This article has an associated First Person interview with the first author of the paper.
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