| First Author | Tone D | Year | 2022 |
| Journal | PLoS Biol | Volume | 20 |
| Issue | 10 | Pages | e3001813 |
| PubMed ID | 36194579 | Mgi Jnum | J:330043 |
| Mgi Id | MGI:7345008 | Doi | 10.1371/journal.pbio.3001813 |
| Citation | Tone D, et al. (2022) Distinct phosphorylation states of mammalian CaMKIIbeta control the induction and maintenance of sleep. PLoS Biol 20(10):e3001813 |
| abstractText | The reduced sleep duration previously observed in Camk2b knockout mice revealed a role for Ca2+/calmodulin-dependent protein kinase II (CaMKII)beta as a sleep-promoting kinase. However, the underlying mechanism by which CaMKIIbeta supports sleep regulation is largely unknown. Here, we demonstrate that activation or inhibition of CaMKIIbeta can increase or decrease sleep duration in mice by almost 2-fold, supporting the role of CaMKIIbeta as a core sleep regulator in mammals. Importantly, we show that this sleep regulation depends on the kinase activity of CaMKIIbeta. A CaMKIIbeta mutant mimicking the constitutive-active (auto)phosphorylation state promotes the transition from awake state to sleep state, while mutants mimicking subsequent multisite (auto)phosphorylation states suppress the transition from sleep state to awake state. These results suggest that the phosphorylation states of CaMKIIbeta differently control sleep induction and maintenance processes, leading us to propose a "phosphorylation hypothesis of sleep" for the molecular control of sleep in mammals. |
