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Early events of multiple bud formation and shoot development in soybean embryonic axes treated with the cytokinin, 6‐benzylaminopurine
Author(s) -
Buising Charisse M.,
Shoemaker Randy C.,
Benbow Robert M.
Publication year - 1994
Publication title -
american journal of botany
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.218
H-Index - 151
eISSN - 1537-2197
pISSN - 0002-9122
DOI - 10.1002/j.1537-2197.1994.tb15630.x
Subject(s) - meristem , biology , axillary bud , cytokinin , shoot , apex (geometry) , apical dominance , organogenesis , cell division , botany , morphogenesis , lateral shoot , microbiology and biotechnology , apical cell , embryonic stem cell , tissue culture , cell , auxin , genetics , in vitro , gene
Early events of multiple bud formation and shoot development in germinating soybean embryonic axes treated for 24 hr with the cytokinin, 6‐benzylaminopurine (BAP), were compared to the development of untreated control axes using four different techniques: photomicrography, scanning electron microscopy, histology, and autoradiography. Shoot apex development in BAP‐treated embryonic axes was delayed by about 9 to 15 hr. A transient inhibition of DNA synthesis in the primary apical meristem and axillary buds was observed with subsequent changes in the timing of cell division patterns in these regions. Meristematic regions (supernumerary vegetative buds) were observed in BAP‐treated axes around the perimeter of the apical dome at and above the level of the axillary buds. Cells elongated from some of the BAP‐induced meristematic regions to form four to six shoots. In the absence of BAP, excision of the primary apical meristem and/or axillary buds did not result in multiple bud formation. These results suggest that transient exposure to BAP interrupted chromosomal DNA replication and reprogrammed the developmental fate of a large number of cells in the shoot apex. We postulate that interruption of DNA synthesis, either directly, by interfering with DNA replication, or indirectly, by preventing entry into S‐phase, effected redetermination of the shoot apex cells.