A B S T RAe TThe dimensions of mericlinal sectors in periclinal chimeras resulting from replacement-displacement phenomena have been used to determine the number of shoot apical initial cells and their mitotic activity. Narrow sectors were always short, extending an average of less than three nodes. All long sectors were wide, involving 3i or Y2 of the circumference of the stem. These observations define the origin of all primary growth as from 1-3 apical initial cells in each of the apical layers. The sectors reveal a surprising stability of cellular position at the center of growth, with a specific initial cell maintaining its position during formation of over 100 nodes. During vigorous vegetative growth of Ligustrum ovalifolium the initials themselves divide only about once in 12 days during the formation of three nodes. The mitotic index of the initials in privet shoot apices is 1.4, and this rate of division is sufficient for them to be the ultimate source of all cells composing the shoot.
The development of leaves on apically stable, periclinal chimeras was studied in a number of dicot genera. The mutant cell layers of the shoot apex and the tissues derived from them were as active developmentally as the normal layers. Ontogeny was the same in these chimeras as in nonchimeras, and growth of their leaves can be outlined as follows. Formation of the buttress, the axis, and the lamina of simple dicot leaves were independent events. In each the first growth included derivatives of the apical layers, usually three in number, found in the apex of the shoot and the lateral buds. Most cell divisions in the outer layers (L‐I and L‐II) were anticlinal relative to the new structures. Therefore, in the proximal regions of the buttress, axis (petiole and midrib), and lamina, the derivative cells of L‐I and L‐II were usually present in single layers. The rest of the internal tissue was from L‐III. As formation of the axis and the lamina proceeded, derivatives of L‐II replaced L‐III internally in the distal and marginal regions leaving cells of L‐III behind. Both the determinate growth of leaves and the pattern of cell divisions at and near the leading edges of growth meant that no cells in the leaf were comparable to the initial cells of the shoot apex. As the lamina extended, there were extensive intercalary cell divisions, both anticlinal and periclinal, so that in any given region of a leaf the layers of internal cells were from either L‐II or L‐III. At any point along the axis, L‐III participated or did not participate in laminar extension. At any given stage in laminar growth either of two sister cells in any internal layer divided either a few times or extensively. The extreme variability in direction and frequency of cell division during leaf development was under an overriding genetic control, which resulted in the normal or typical size, shape and thickness of leaves.
A mosaic pattern of leaf variegation in a sector on a normal green tobacco seedling resulted from maturation of both green and white cells within the tissue derived from the second histogenic layer (L–II) of the shoot apex. While mature cells of L–II origin contained either green plastids or colorless plastids, single cells in young leaves contained both normal green plastids and colorless, defective mutant plastids. The genetic determiner of the defective plastid type, designated DP1, was located in the plastid itself. Only a small number of mutant plastids were found in anyone cell. A threshold number of DP1 above which green plastids were inhibited and below which they developed normally is suggested. Random segregation of DP1 and dP1 in cytokinesis, close to the threshold value and without loss of either determiner, could account for the small, intermingled patches of green and white cells derived from the mosaic histogenic layer. The mosaic histogen usually remained mosaic; however, complete segregation during mitosis to DP1 or dP1 occasionally occurred in sectors within which lateral buds developed in a stabilized condition, either normal or mutant (green or white). Occasional replacement of L–III by L–II apparently introduced the mosaic condition into L–III of the original variegated plant and resulted in an additional pattern of variegation. Patterns of variegation in which the sporogenous tissue was derived from a stable L–II with homoplastidic cells produced only green or only white offspring. Variegated seedlings were obtained only when L–II was mosaic. Contrasting statements on the inheritance of variegations appearing in the literature result from failure to describe accurately the pattern of variegation. Description in terms of plastid types in mature histogens is essential, and plastid segregation in somatic tissue of mosaic L–II must be determined. Variegation should only be used as a general term and further described as stable when the histogens are homoplastidic or mosaic when the histogens are heteroplastidic. Complete description of the inheritance of a plastid mutant must record inclusion or loss in successive cell generations of sexual seedlings. DP1 is inherited only maternally and is found in fewer of the offspring than expected on the basis of its segregation in mitosis. When present in the egg cell and, therefore, the zygote, DP1 can be included in all 3 histogenic layers of the seedling, thereby producing many more variegated patterns than were possible from the original mosaic plant.
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