The Arabidopsis (Arabidopsis thaliana) gynoecium, the female floral reproductive structure, requires the action of genes that specify positional identities during its development to generate an organ competent for seed development and dispersal. Early in gynoecial development, patterning events divide the primordium into distinct domains that will give rise to specific tissues and organs. The medial domain of the gynoecium gives rise to the ovules, and several other structures critical for reproductive competence. Here we report a synergistic genetic interaction between seuss and aintegumenta mutants resulting in a complete loss of ovule initiation and a reduction of the structures derived from the medial domain. We show that patterning events are disrupted early in the development of the seuss aintegumenta gynoecia and we identify PHABULOSA (PHB), REVOLUTA, and CRABS CLAW (CRC) as potential downstream targets of SEUSS (SEU) and AINTEGUMENTA (ANT) regulation. Our genetic data suggest that SEU additionally functions in pathways that are partially redundant and parallel to PHB, CRC, and ANT. Thus, SEU and ANT are part of a complex and robust molecular system that coordinates patterning cues and cellular proliferation along the three positional axes of the developing gynoecium.During organ development, positional identity information must be coordinated with cellular proliferation to achieve proper organ shape and function. In the Arabidopsis (Arabidopsis thaliana) gynoecium, the female reproductive floral structure, early patterning events divide the gynoecial primordium into distinct zones that distinguish adaxial (inner) versus abaxial (outer), medial versus lateral, and apical versus basal

Multimeric protein complexes are required during development to regulate transcription and orchestrate cellular proliferation and differentiation. The Arabidopsis (Arabidopsis thaliana) SEUSS (SEU) gene encodes a transcriptional adaptor that shares sequence similarity with metazoan Lim domain-binding transcriptional adaptors. In Arabidopsis, SEU forms a physical complex with the LEUNIG transcriptional coregulator. This complex regulates a number of diverse developmental events, including proper specification of floral organ identity and number and the development of female reproductive tissues derived from the carpel margin meristem. In addition to SEU, there are three Arabidopsis SEUSS-LIKE (SLK) genes that encode putative transcriptional adaptors. To determine the functions of the SLK genes and to investigate the degree of functional redundancy between SEU and SLK genes, we characterized available slk mutant lines in Arabidopsis. Here, we show that mutations in any single SLK gene failed to condition an obvious morphological abnormality. However, by generating higher order mutant plants, we uncovered a degree of redundancy between the SLK genes and between SLK genes and SEU. We report a novel role for SEU and the SLK genes during embryonic development and show that the concomitant loss of both SEU and SLK2 activities conditions severe embryonic and seedling defects characterized by a loss of the shoot apical meristem. Furthermore, we demonstrate that SLK gene function is required for proper development of vital female reproductive tissues derived from the carpel margin. We propose a model that posits that SEU and SLK genes support organ development from meristematic regions through two different pathways: one that facilitates auxin response and thus organ initiation and a second that sustains meristematic potential through the maintenance of SHOOTMERISTEM-LESS and PHABULOSA expression.

In flowering plants the gynoecium is the female reproductive structure and the site of oogenesis, fertilization, and maturation of the embryo and the seed. Proper development of the gynoecium requires that the early gynoecial primordium be partitioned into distinct spatial domains with divergent fates. Regulated transport of the phytohormone auxin previously has been shown to play a role in the patterning of spatial domains along the apical-basal axis of the gynoecium. Here we establish a role for auxin transport in patterning along the medio-lateral axis of the gynoecial ovary. We demonstrate that auxin transport is required for the development of the medial ovary domain that contains the carpel margin meristem, a vital female reproductive structure. Disruptions in auxin transport enhance the medial domain defects observed in aintegumenta and revoluta mutant genotypes. Aintegumenta and revoluta are likely to function in parallel and partially overlapping pathways required for medial domain development. Our data indicate that different ovary domains are differentially sensitive to the reduction of polar auxin transport and the loss of aintegumenta and revoluta activity. We suggest that an auxin-mediated positional cue is important for the differential specification of the medial and lateral ovary domains.