Microtubules and lithocyst morphogenesis in Pilea cadierei

Abstract

Lithocysts in Pilea cadierei are initiated by differential divisions, the plane of which is predicted by typical preprophase microtubule bands. They soon become polarized and undergo a unique differentiation. The external periclinal wall thickens considerably in the absence of microtubules. In incipient lithocysts, a periclinal band of microtubules lines the external ends of the anticlinal walls. A distinct local thickening, possessing periclinal cellulose microfibrils, underlies the microtubule band. The cystolith stalk originates as a cylindrical wall ingrowth of a limited central region of the external periclinal wall. This grows inwards in the absence of microtubules in a preformed cytoplasmic diaphragm, approaching the internal periclinal wall. Stalk formation as well as the external periclinal wall thickening are not affected by colchicine and isopropyl n(3-chlorophenyl) carbamate. A cystolith body is formed within a cytoplasmic diaphragm in which most of the lithocyst organelles are located; this body is rich in cellulose microfibrils and is formed by the deposition of large amounts of wall material at the free end of the stalk, at right angles to its axis. This morphogenetic shift is preceded by the formation of a system of microtubules that converge in cortical sites close to the stalk. They proliferate and form an axial sheath around the cystolith body. The cellulose microfibrils are aligned in a parallel fashion with microtubules. Microtubule destruction by colchicine results in malformation of both the lithocyst and the cystolith body. Aberrant cystolith bodies are also formed in the presence of isopropyl n(3-chlorophenyl) carbamate, which seems to interfere with microtubule formation. These observations suggest that the lithocyst – cystolith body morphogenesis is controlled by microtubules.