The tailless ortholog nhr-67 functions in the development of the C. elegans ventral uterus.

The development of the C. elegans uterus provides a model for understanding the regulatory pathways that control organogenesis. In C. elegans, the ventral uterus develops through coordinated signaling between the uterine anchor cell (AC) and a ventral uterine (VU) cell. The nhr-67 gene encodes the nematode ortholog of the tailless nuclear receptor gene. Fly and vertebrate tailless genes function in neuronal and ectodermal developmental pathways. We show that nhr-67 functions in multiple steps in the development of the C. elegans uterus. First, it functions in the differentiation of the AC. Second, it functions in reciprocal signaling between the AC and an equipotent VU cell. Third, it is required for a later signaling event between the AC and VU descendants. nhr-67 is required for the expression of both the lag-2/Delta signal in the AC and the lin-12/Notch receptor in all three VU cells and their descendants, suggesting that nhr-67 may be a key regulator of Notch-signaling components. We discuss the implications of these findings for proposed developmental regulatory pathways that include the helix-loop-helix regulator hlh-2/daughterless and transcription factor egl-43/Evi1 in the differentiation of ventral uterine cell types.

The histone acetyltransferase GCN5 affects the inflorescence meristem and stamen development in Arabidopsis.

A central question in biology is to understand how gene expression is precisely regulated to give rise to a variety of forms during the process of development. Epigenetic effects such as DNA methylation or histone modification have been increasingly shown to play a critical role in regulation of genome function. GCN5 is a prototypical histone acetyltransferase that participates in regulating developmental gene expression in several metazoan species. In Arabidopsis thaliana, plants with T-DNA insertions in GCN5 (also known as HAG1) display a variety of pleiotropic effects including dwarfism, loss of apical dominance, and floral defects affecting fertility. We sought to determine when during early development floral abnormalities first arise. Using scanning electron microscopy, we demonstrate that gcn5-1/hag1-1 and gcn5-5/hag1-5 mutants display overproliferation of young buds and development of abnormal structures around the inflorescence meristem. gcn5 mutants also display defects in stamen number and arrangement at later stages. This analysis provides temporal and spatial information to aid in the identification of GCN5 target genes in the developing flower. Preliminary studies of putative targets using reverse transcriptase PCR suggest that the floral meristem identity gene LEAFY is among factors upregulated in gcn5-1 mutants.