Effect of neuron-specific short-form ATF6 overexpression on gene expression in the mouse brain

One major component of cellular proteome resides in the endoplasmic reticulum (ER), the key organelle for protein biogenesis in the secretory pathway. Disruption of ER proteostasis leads to ER stress, which subsequently activates multiple adaptive stress response pathways, collectedly termed as the unfolded protein response (UPR). One UPR branch is mediated by ATF6 (activating transcription factor 6). Activation of the ATF6 branch generates a transcriptional factor: short form ATF6 (sATF6). Since activation of this UPR branch has been shown to be neuroprotective in brain ischemia/stroke, it is critical to identify what genes are regulated by the sATF6 in neurons in vivo and determine the molecular mechanisms underlying the beneficial effects exerted by this UPR branch. In this study, we performed RNA-Seq analysis on the hippocampus from sATF6 conditional transgenic mice. Compare gene expression between control (Emx-Cre) mice and sATF6 conditional knock-in (sATF6-KI; Rosa26-sATF6-MER;Emx1-Cre ) mice (n =3).