Several earlier studies in vivo and in vitro suggest that the occurrence of tubular ER depends on an intactactomyosin system in plant cells. Any interference with the actomyosin system (disintegration of the actin filaments by cytochalasin D; the inactivation of myosin by use of the ionophore calcimycin to elevate or lower the calcium concentration to an unfavourable level; artificially crosslinking myosin with actin filaments by NEM) results in the loss of tubular elements and the formation of large flat sheet-like ER sacs. Previously-formed flat sheet-like ER sacs, however, split into ER tubules after lowering the cytosolic pH by loading with a weak acid or simply by chilling the epidermis cells, although the actomyosin system is still inactivated by either cytochalasin D, calcimycin, or NEM. Our results provide strong evidence that the actomyosin system is not necessarily involved in the formation of tubular ER which, most likely, is an intrinsic property of the ER membrane. A possible role for protons and! or calcium is discussed.