In maize (Zea mays), sex determination occurs through abortion of female carpels in the tassel and arrest of male stamens in the ear. The Tasselseed6 (Ts6) and tasselseed4 (ts4) mutations permit carpel development in the tassel while increasing meristem branching, showing that sex determination and acquisition of meristem fate share a common pathway. We show that ts4 encodes a mir172 microRNA that targets APETALA2 floral homeotic transcription factors. Three lines of evidence suggest that indeterminate spikelet1 (ids1), an APETALA2 gene required for spikelet meristem determinacy, is a key target of ts4. First, loss of ids1 suppresses the ts4 sex determination and branching defects. Second, Ts6 mutants phenocopy ts4 and possess mutations in the microRNA binding site of ids1. Finally, IDS1 protein is expressed more broadly in ts4 mutants compared to wild type. Our results demonstrate that sexual identity in maize is acquired by limiting floral growth through negative regulation of the floral homeotic pathway.

Abscission is a universal and dynamic process in plants whereby organs such as leaves, flowers and fruit are shed, both during normal development, and in response to tissue damage and stress. Shedding occurs by separation of cells in anatomically distinct regions of the plant, called abscission zones (AZs). During abscission, the plant hormone ethylene stimulates cells to produce enzymes that degrade the middle lamella between cells in the AZ. The physiology and regulation of abscission at fully developed AZs is well known, but the molecular biology underlying their development is not. Here we report the first isolation of a gene directly involved in the development of a functional plant AZ. Tomato plants with the jointless mutation fail to develop AZs on their pedicels and so abscission of flowers or fruit does not occur normally. We identify JOINTLESS as a new MADS-box gene in a distinct phylogenetic clade separate from those functioning in floral organs. We propose that a deletion in JOINTLESS accounts for the failure of activation of pedicel AZ development in jointless tomato plants.

Unlike monopodial plants, in which flowering terminates growth of a shoot, plants exhibiting sympodial shoot architecture maintain the potential for indeterminate growth even after converting to floral development. This vegetative indeterminacy is conferred by a special type of axillary meristem, the sympodial meristem, which exhibits precocious but determinate growth. The reiterative formation of sympodial meristems as the plant grows results in a shoot composed of a series of modules, each consisting of a limited number of vegetative nodes and terminated by a flower or inflorescence. To determine how sympodial meristems differ from other shoot meristems, we examined interactions between mutations that affect various shoot meristem types in tomato (Lycopersicon esculentum Mill.). Analysis of double mutant combinations of jointless, lateral suppressor, self-pruning, blind, and anantha showed that sympodial meristems share regulatory features with inflorescence meristems. Genetic studies on the jointless mutation implicated this gene in suppressing sympodial meristem fate in the inflorescence. As this mutation has a second phenotype, the elimination of the pedicel abscission zone, we examined the expression pattern of JOINTLESS to test whether pedicel development is involved in directing shoot architecture. We found that this MADS box gene is expressed in a variety of shoot meristems, including inflorescence, floral, sympodial, and axillary meristems, as well as in early staged floral organs, in sporogenous tissues of anthers, and in ovules. Lack of expression in developing pedicels indicates abscission zone development does not rely on JOINTLESS transcription in the differentiating cells. We conclude that the primary role of JOINTLESS is to suppress sympodial meristem identity in inflorescence meristems.

The tassel seed mutations ts4 and Ts6 of maize cause irregular branching in its inflorescences, tassels, and ears, in addition to feminization of the tassel due to the failure to abort pistils. A comparison of the development of mutant and wild-type tassels and ears using scanning electron microscopy reveals that at least four reproductive meristem types can be identified in maize: the inflorescence meristem, the spikelet pair meristem, the spikelet meristem, and the floret meristem. ts4 and Ts6 mutations affect the fate of specific reproductive meristems in both tassels and ears. ts4 mutants fail to form spikelet meristems from spikelet pair meristems. Ts6 mutants are delayed in the conversion of certain spikelet meristems into floret meristems. Once floret meristems are established in both of these mutants, they form florets that appear normal but fail to undergo pistil abortion in the tassel. The abnormal branching associated with each mutant is suppressed at the base of ears, permitting the formation of normal, fertile spikelets. The classification of the different types of reproductive meristems will be useful in interpretation of gene expression patterns in maize. It also provides a framework for understanding meristem functions that can be varied to diversify inflorescence architectures in the Gramineae.

The tassel seed mutations of maize cause sex reversal of the florets of the tassel, such that the normally staminate florets develop pistils. Although these mutations have been recognized for many years, little is known about how they act. We have tested the hypothesis that the tassel seed genes interact directly with each other and with other genes controlling sex determination in a single genetic pathway by the construction and analysis of double mutants. On the basis of the phenotypes of the double mutants, the tassel seed mutations were placed into two groups: ts1, ts2, Ts5 and ts4, Ts6. Both groups of tassel seed mutations were additive with the masculinizing mutation dwarf, indicating independent modes of action. Interactions of tassel seed mutations with silkless varied, allowing the ordering of the action of the various tassel seed mutations relative to silkless. Both groups of tassel seed mutations were epistatic with regard to sex expression to mutations that alter both architecture of the plant and distribution of male and female florets, Teopod 1, terminal ear, and teosinte branched. Thus, there are at least two separate genetic pathways that control the sex of florets in maize tassels. In addition, analysis of double mutants revealec that all tassel seed genes tested play a role in the regulation of flower morphogenesis as well as pistil suppression. © 1994 Wiley‐Liss, Inc.