Six different homoplastidic periclinal chimeras of tobacco carrying the plastogene DP1 were selected after somatic segregation in heteroplastidic seedlings. Direct observation of the plane of division in epidermal cells of young leaves, and the number and size of sub‐epidermal green spots on leaves with the Green‐White‐White (G‐W‐W) pattern of variegation, indicated that the ratio of periclinal to anticlinal divisions in L‐I during development of the lamina was 1:3100. The number of green and white seedlings obtained from the different chimeral branches indicated a similar frequency of periclinal divisions in development of the ovary. The arrangement of green and white tissue in mature leaves of the various chimeral types indicated the extent of participation by the three apical layers in the initiation of the buttress, development of the axis, and formation of the lamina. During development of the lamina there must be three independent initial‐groups present. L‐I and L‐II initials remain marginal, but early in the growth of the lamina the leading edge of tissue derived from L‐III becomes separated from the submarginal (L‐II) initials by the products of frequent periclinal divisions of the L‐II initials.

Abundant seeds of high germinability are obtained when Nicotiana tabacum is pollinated by Nicotiana africana. Most of the seedlings die at the cotyledonary stage. The remaining seedlings are viable F(1) hybrids or maternal haploids that can be easily distinguished. This simple method of producing Nicotiana tabacum haploids offers an alternative to anther culture.

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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Low activity of 5'-nucleotidase (5'-ribonucleotide phosphohydrolase, EC 3.1.3.5) in T lymphoblasts may explain the marked sensitivity of this cell to deoxynucleotide accumulation when compared to B Iymphoblasts. The relevance of such observations with cultured cells to the normal immune system requires the demonstration of similar differences in the 5'-nucleotidase activity of normal human lymphocyte subpopulations. Sheep erythrocyte (E) rosette-forming cells from normal thymus, tonsi , and peripheral mononuclear cells have 5'-nucleotidase activities of 1.7, 11.3, and 21.2 nmol/hr per 106 cells. Non-E-rosette forming cells from the peripheral blood or tonsil have 5'-nucleotidase activity comparable to the higher levels found in the peripheral E-RFC. Increased levels of5'-nucleotidase activity may be a marker for post-thymic T Iymphocytes.T lymphoblasts have 5'-nucleotidase activity similar to values demonstrated for E-RFC in thymus, whereas cultured B lymphoblasts have 5'-nucleotidase activity 15 times greater than that of T lymphoblasts. On the basis of these observations, the 5'-nucleotidase deficiency in congenital agammaglobulinemia has been reevaluated. In these patients the data indicate that peripheral E-rosette forming cells have the enzyme deficiency, demonstrating an abnormality of T lymphocytes in this disorder of immunoglobulin production. Lymphocyte 5'-nucleotidase (5'-ribonucleotide phosphohydrolase, EC 3.1.3.5) may have an important role in the regulation of the human immune system. Decreased activity of this purine catabolic enzyme has been observed in patients with primary immunoglobulin deficiency (1-4). However, it remains unclear whether an etiological relationship exists between the immune dysfunction and this enzyme deficiency.A marked difference in 5'-nucleotidase activity has been proposed as the molecular basis for the differential susceptibility of B and T lymphoblast lines to the toxicity related to deoxynucleoside accumulation (5-7). T lymphoblasts are killed by deoxyadenosine or deoxyguanosine, rapidly accumulate dATP or dGTP, and have very low levels of 5'-nucleotidase (5-9). In contrast, B lymphoblasts grow normally in deoxyadenosine or deoxyguanosine, accumulate only small quantities of deoxynucleoside triphosphates, and have higher 5'-nucleotidase levels than T lymphoblasts (5-9 and four T lymphoblast lines (CEM, Jurkat, MSB-2, and MOLT-3) were maintained and characterized as described (10).Peripheral lymphocytes were obtained, separated into Erosette forming cells and non-E-rosette forming cells, and characterized by described methods (11)(12)(13). Lymphoid organs were obtained from children with no known immune dysfunction, and cells were separated from these tissues within 1 hr of surgery by using described methods (14)

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The gross morphological effects of the herbicide 4-methyl-sulphonyl-2,6-dinitro-N,N-dipropylaniline [nitralin] on roots of corn (Zea mays L., var. U. S. 13) suggested abnormal cytological behavior. Roots of corn plants treated preemergence with nitralin developed digitate to globose swelling in the region of active cell division of the root tip. Cytological examination of the affected area showed that the effects of the herbicide were prevention of cell wall formation, enlargement of cells, and extensive replication of nuclei, and suggests that a primary effect of nitralin is on cell division and that this may be a primary mechanism of action as a herbicide.

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