ABSTRACT IN this paper the width of the stomatal aperture, as postulated by von Mohl in 1856, is shown to be a function of the hydrostatic (turgor) pressure in the guard cells, Pg, and the pressure, Ps, of the immediately surrounding epidermal cells, which will be referred to as the subsidiary cells in this paper. The aperture does not depend solely upon the pressure difference (Pg-Ps) as believed by Ursprung and Blum (1924) and StSlfelt (1966). Instead, aperture width is shown to be a simple multi-linear relationship (i.e., a linear com-bination) of Pg and Ps. The recent re-search by Glinka (1971) and Edwards, Meidner and Sheriff (1976), showing the relative contributions of the oppos-ing pressures Pg and Ps, is, thus, given a simple and lucid interpreta-tion. The analysis of a guard cell as an elliptical torus shows that a stomate could function without either of the two conditions classically believed to be essential (Meyer et al. 1960, p. 84, Meidner and Mansfield 1968, pp. 14-17, Bidwell 1974, p. 298). The thick-ened wall (ventral wall) of the guard cell facing the aperture need not neces-sarily be stiffer than the dorsal wall common to the adjacent epidermal cell for the proper functioning of a stomate. The radially oriented cellu-lose microfibrils in the guard cell wall are not vital but are important for quite different reasons than claimed by Aylor et al. (1973). Consideration of the radial stiffening by means of the in-troduction of a mechanically equiva-lent orthogonally anisotropic (i.e., or-thotropic) material causes the aperture width to be more sensitive to a unit increment in Ps than to a unit incre-ment in Pg (for parameters of physi-cal interest3). The guard cell volume, however, is smaller than the adja-cent cell volume and Pg is believed to be larger than Ps, in general. We conjecture that this increased sensi-tivity for the subsidiary cell (i.e., clos-ing) pressure is important for the functioning of the feedback control loops regulating the aperture width. We define an antagonism ratio to characterize this property. The pore length in the model is shown to be surprisingly constant during opening, as is reported for many species (Meidner and Mansfield 1968, p. 12). The guard cell is generally believed to bulge into the neighboring epider-mal cell upon opening (Meidner and Mansfield 1968, p. 15). However, the shell model suggests that the outer-most portion of the guard cell at the widest point (and not visible in an in vivo situation) actually moves away from the neighboring cell. The ap-proximate point at which the exposed surface of the epidermal cell joins the guard cell exhibits only limited mo-tion. Note that there are especially thin regions here in the epidermal cell thought to behave as hinges (Hautgelenke). Even when the ex-treme, unphysiological case of a fixed aperture length is imposed, the outermost perimeter moves away from the adjacent cell. If the epidermis is opaque, the view from outside the leaf suggests that the guard cell bulges into the neighboring cell, as claimed in the classical hypothesis, provided the stiffening effect of the micellae is sufficiently prominent and provided the guard cell pressure is significantly larger than the epidermal cell pres-sure. The opposing influence of the turgor pressure in the guard cells and in the adjacent epidermal cells is shown to be an inherent part of the stomatal mechanism (von Mohl 1856). Pressure influence coefficients for the guard cell are defined and related to parameter changes, e. g., material and thickness. The multilinear relationship of aperture width to the opposing turgor pressures was found and revealed that pore width does not depend solely on the pressure difference between the guard cell and the adjacent epidermal cell. Finally, the theory developed is shown to embrace and to clarify the experimental results of Glinka's plas-molytic study (1971) and the direct method of Edwards et al. (1976).
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