Abstract

Plastid primordia in the root tips of Zea mays are mitochondria. In the root cap their development into mature plastids can be traced within a single microscopic field. In the region of differentiation of the root proper two distinct types of mitochondria occur, the larger of which develops into plastids while the smaller apparently undergoes no further change. In the stem growing point the primordia are generally minute plastids, that is, hollow spheroids containing starch grains 0.5 μ in diameter in the central vacuoles, although occasionally they are mitochondria. Back from the growing point of the stem in the epicotyl, the primordia quickly develop into plastids. In the procambial cells plastid-like bodies can be observed to fragment, and there is some evidence that these fragments develop into mitochondria. In the vascular bundles many transitional stages can be observed in the course of development of mitochondria into plastids. In the leaves the primordia develop into mitochondria in the phloem, into large starch-containing plastids with prominent pores in the cells immediately surrounding the vascular bundles, and into smaller, apparently denser plastids in the chlorenchymous cells between the bundles. In all aberrant types investigated, the plastid primordia were normal so far as could be observed, the divergent types being due to (1) a delayed development, (2) a stoppage of the development, and (3) a stoppage of development followed by degeneration. In the first albino stock investigated the mode of development in the young plastids suggested an influence exerted by the genetic constitution of the mother plant. A disintegration of the partly developed plastids in the leaves of this stock occurred in all except the earliest-formed cells of the foliage tissue, that is, the tips of the first, second, and third leaves. The second albino stock was evidently an extreme case of virescence. All of the mesophyll tissue of the leaves contained minute plastids. Both albino stocks died while starch was still stored in the epicotyl, indicating that starvation was not the primary cause of death. The divergent plastids in the maternal inheritance stock developed as in normal tissue until they were about half-grown. The first signs of abnormality were not in the plastids themselves but in their number and arrangement within the cells. In tissue of half-grown leaves, a distinct size difference could be observed between the plastids in the light and the dark stripes. In old tissue the plastids in the lighter areas degenerated and disappeared. Mature leaves showed but two kinds of plastids, and contained no intermediate forms on the border-line of the two regions. In the green-yellow lethal stock the plastids degenerated after reaching one-fourth the normal diameter. In "aurea" plastid development was quite normal except for the pigment content. In both the "argentea" and the expallescent-virescent stock the abnormality was due to a checking of plastid development early in the life of the seedling, and to the later normal plastid growth. In general, the abnormal period was between the formation of the tip of the first leaf and the formation of the base of the fifth leaf. Both stocks were very variable.

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