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.