The circadian leaf opening and closing (nyctinasty) of Fabaceae has attracted scientists' attention since the era of Charles Darwin. Nyctinastic movement is triggered by the alternate swelling and shrinking of motor cells at the base of the leaf. This， in turn， is facilitated by changing osmotic pressures brought about by ion flow through anion and potassium ion channels. However， key regulatory ion channels and molecular mechanisms remain largely unknown. Here， we identify three key ion channels in mimosoid tree Samanea saman: the slow-type anion channels， SsSLAH1 and SsSLAH3， and the Shaker-type potassium channel， SPORK2. We show that cell-specific circadian expression of SsSLAH1 plays a key role in nyctinastic leaf opening. In addition， SsSLAH1 co-expressed with SsSLAH3 in flexor (abaxial) motor cells promoted leaf opening. We confirm the importance of SLAH1 in leaf movement using SLAH1-impaired Glycine max. Identification of this "master player" advances our molecular understanding of nyctinasty.