In higher plants, organogenesis occurs continuously from self-renewing apical meristems. Arabidopsis thaliana plants with loss-of-function mutations in the CLAVATA (CLV1, 2, and 3) genes have enlarged meristems and generate extra floral organs. Genetic analysis indicates that CLV1, which encodes a receptor kinase, acts with CLV3 to control the balance between meristem cell proliferation and differentiation. CLV3 encodes a small, predicted extracellular protein. CLV3 acts nonautonomously in meristems and is expressed at the meristem surface overlying the CLV1 domain. These proteins may act as a ligand-receptor pair in a signal transduction pathway, coordinating growth between adjacent meristematic regions.

Development in higher plants depends on the activity of meristems, formative regions that continuously initiate new organs at their flanks. Meristems must maintain a balance between stem cell renewal and organ initiation. In fasciated mutants, organ initiation fails to keep pace with meristem proliferation. The thick tassel dwarf1 (td1) mutation of maize affects both male and female inflorescence development. The female inflorescence, which results in the ear, is fasciated, with extra rows of kernels. The male inflorescence, or tassel, shows an increase in spikelet density. Floral meristems are also affected in td1 mutants; for example, male florets have an increase in stamen number. These results suggest that td1 functions in the inflorescence to limit meristem size. In addition, td1 mutants are slightly shorter than normal siblings, indicating that td1 also plays a role in vegetative development. td1 encodes a leucine-rich repeat receptorlike kinase (LRR-RLK) that is a putative ortholog of the Arabidopsis CLAVATA1 protein. These results complement previous work showing that fasciated ear2 encodes a CLAVATA2-like protein, and suggest that the CLAVATA signaling pathway is conserved in monocots. td1 maps in the vicinity of quantitative trait loci that affect seed row number, spikelet density and plant height. We discuss the possible selection pressures on td1 during maize domestication.Key words: Meristem, Stem cells, Inflorescence, thick tassel dwarf1, Maize Summary thick tassel dwarf1 encodes a putative maize ortholog of the Arabidopsis

Mutations in the PERIANTHIA (PAN) gene of Arabidopsis thaliana specifically transform flowers from tetramerous to largely pentamerous, which is a characteristic of flowers of ancestral plants. We have cloned the PAN gene and here we show that it encodes a member of the basic region/leucine zipper class of transcription factors. Immunohistochemical analysis shows that the encoded protein is present in the apical meristem, the floral meristem, each whorl of organ primordia, and in ovule primordia during wild-type flower development. PAN expression occurs independently of genes affecting floral meristem identity, floral meristem size, or floral organ number. The near absence of a phenotype in transgenic plants overexpressing PAN and the contrast between the broad expression of PAN and the specificity of its mutant phenotype suggest that its activity may be regulated post-translationally or by the presence of partner proteins. Based on these results and on data reported previously, we propose models for the role of PAN in the evolution of flower pattern in the mustard family. Arabidopsis flowers arise initially as undifferentiated bulges on the flank of the apical meristem. Soon afterward, whorls of organ primordia arise sequentially. Four sepal primordia develop along the edges of the floral meristem, establishing the first whorl. Then four petal and six stamen primordia initiate in whorls 2 and 3, respectively, followed by development of two carpel primordia in the center of the floral meristem (Smyth et al. 1990).A proposed mechanism of floral organ primordium initiation and formation must account for how a primordium is formed and also when and where on the floral meristem it develops. The eventual fate of organ primordia is determined by the organ identity genes (Komaki et al. 1988;Bowman et al. 1989Bowman et al. , 1991Bowman et al. , 1993Hill and Lord 1989;Kunst et al. 1989;Irish and Sussex 1990;Jack et al. 1992;Weigel and Meyerowitz 1994); however, the position in which they arise (and thus their number) appears to be established independently (Meyerowitz 1997). How proper floral organ number is achieved is not well understood.One way to understand the molecular mechanisms by which appropriate floral organ number is determined is to find mutations that affect floral organ number but do not affect floral organ identity or floral meristem identity, and then to elucidate the nature and the function of the corresponding wild-type genes. There are a number of reports demonstrating the existence of such muta-, and wiggum (wig) (Leyser and Furner 1992;Clark et al. 1993Clark et al. , 1995Clark et al. , 1997Roe et al. 1993Roe et al. , 1997Sessions and Zambryski 1995;Talbert et al. 1995;Running and Meyerowitz 1996;Sessions et al. 1997;Laufs et al. 1998;Kayes and Clark 1998;Running et al. 1998). In clv1, clv3, and wig mutants, the increase in organ number is correlated with increased cell number in the floral meristem (Clark et al. 1993(Clark et al. , 1995Running et al. 1998). This indicates a mechanism by which the pos...

Meristems require a myriad of intercellular signaling pathways for coordination of cell division within and between functional zones and clonal cell layers. This control of cell division ensures a constant availability of stem cells throughout the life span of the meristem while limiting overproliferation of meristematic cells and maintaining the meristem structure. We have undertaken a genetic screen to identify additional components of meristem signaling pathways. We identified pluripetala (plp) mutants based on their dramatically larger meristems and increased floral organ number. PLURIPETALA encodes the ␣-subunit shared between protein farnesyltransferase and protein geranylgeranyltransferase-I. plp mutants also have altered abscisic acid responses and overall much slower growth rate. plp is epistatic to mutations in the ␤-subunit of farnesyltransferase and shows a synergistic interaction with clavata3 mutants. plp mutants lead to insights into the mechanism of meristem homeostasis and provide a unique in vivo system for studying the functional role of prenylation in eukaryotes.