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The Mechanism of Colchicine-Induced Cytohistological Changes in Cranberry

Haig Dermen
American Journal of Botany
Vol. 32, No. 7 (Jul., 1945), pp. 387-394
Stable URL: http://www.jstor.org/stable/2437356
Page Count: 8
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The Mechanism of Colchicine-Induced Cytohistological Changes in Cranberry
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Abstract

When cranberry plants are treated with colchicine to induce polyploidy, the results are mostly chimeric polyploids of sectorial and periclinal type. The present article reports a cytohistological study of the mechanism underlying the development of such polyploid sectorial and periclinal chimeras. In the apical domes of runner-branch tips and of axillary buds there are three primary histogenic layers. Although the cells of these layers are alike, the layers appear to be histogenetically independent, each usually giving rise to a specific tissue or tissues. The apparent histogenetic independence of the layers seems to be determined by the direction of cell division, particularly in the cells at the summit of the apical dome. The cells of the dome in the two outermost layers, L-I and L-II, divide anticlinally, hence their uniseriate appearance, whereas those of layer III divide both anticlinally and periclinally. Thus, because of the way in which they divide, these layers seem to remain distinct and independent. Whether the anticlinal mode of division, particularly in the cells at the summit of the apical dome, sometimes changes into periclinal in either L-I or L-II is being investigated further. One, two, or usually a maximum of three cells seem to maintain a central position in each histogenic layer at the summit of the dome, and to perform the function of carrying out histogenetic continuity of each layer. One or more of these centrally located cells in any of the three layers may become polyploidized by colchicine treatment, the other cells remaining normal. When not all of the central cells in a given layer have been polyploidized, the tissues produced from this layer show sectorial polyploidy, which may be independent in each layer. Because not more than three cells generally seem to hold a central position at the apical dome, continuous polyploid sectors might be expected to occupy either approximately one-third, one-half, or two-thirds of the circumference or mass of a stem tissue derived from a particular histogenic layer. Polyploidy may affect in toto one or two of the three histogenic layers, the remaining layers being normal. Such a concentric development results in periclinal polyploidy. Polyploidy resulting from colchicine treatment may be classified into two types: apical and axial. The former results from colchicine effect in central cells of any of the histogenic layers at the apical dome; the latter denotes polyploidy in other than central cells. Apical polyploidy results in continuous polyploidy in that portion of the growing stem resulting from those central apical cells that were polyploidized. Axial polyploidy is of localized nature and delimited in its extent. It changes to apical polyploidy only when buds arise in such localized polyploid tissue. Some cytohistological and cytomorphological data for cranberry are presented in respect to the apical dome; the points of origin of leaf primoridia; the number of leaf scales and leaf primordia in axillary buds; the number of leaf primordia, young leaves, and mature leaves at certain distances from the center of the apical dome of runner branches; and phyllotactic arrangement of leaves. These data are used to determine the location of axial and apical polyploidy in branches following bud and stem-tip treatments. In cranberry it seems that a branch arising from a treated axillary bud or stem tip should reach some 30 centimeters or more before sectorial polyploidy derived from apical polyploidy may be recognized. Complete polyploidy in one, two, or three primary histogenic layers may be recognized in shorter branches than in the case of sectorials. It is suggested that in woody plants, if the treatment of a bud results in polyploidy, axial polyploidy will be found in the shoot of the first year's growth, whereas apical polyploidy will be found in the growth of the second or third year unless the treated bud is forced during the first year to make the equivalent of two or more years of growth.

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