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The transcription factors LEAFY (LFY) and APETALA1 (AP1), together with the AP1 paralog CAULIFLOWER (CAL), control the onset of flower development in a partially redundant manner. This redundancy is thought to be mediated, at least in part, through the regulation of a shared set of target genes. However, whether these genes are independently or cooperatively regulated by LFY and AP1/CAL is currently unknown. To better understand the regulatory relationship between LFY and AP1/CAL and to obtain deeper insights into the control of floral initiation, we monitored the activity of LFY in the absence of AP1/CAL function. We found that the regulation of several known LFY target genes is unaffected by AP1/CAL perturbation, while others appear to require AP1/CAL activity. Furthermore, we obtained evidence that LFY and AP1/CAL control the expression of some genes in an antagonistic manner. Notably, these include key regulators of floral initiation such as (), which had been previously reported to be directly repressed by both LFY and AP1. We show here that expression is suppressed by AP1 but promoted by LFY. We further demonstrate that LFY has an inhibitory effect on flower formation in the absence of AP1/CAL activity. We propose that LFY and AP1/CAL act as part of an incoherent feed-forward loop, a network motif where two interconnected pathways or transcription factors act in opposite directions on a target gene, to control the establishment of a stable developmental program for the formation of flowers.

A large fraction of plant genomes is composed of transposable elements (TE), which provide a potential source of novel genes through "domestication"-the process whereby the proteins encoded by TE diverge in sequence, lose their ability to catalyse transposition and instead acquire novel functions for their hosts. In Arabidopsis, ANTAGONIST OF LIKE HETEROCHROMATIN PROTEIN 1 (ALP1) arose by domestication of the nuclease component of Harbinger class TE and acquired a new function as a component of POLYCOMB REPRESSIVE COMPLEX 2 (PRC2), a histone H3K27me3 methyltransferase involved in regulation of host genes and in some cases TE. It was not clear how ALP1 associated with PRC2, nor what the functional consequence was. Here, we identify ALP2 genetically as a suppressor of Polycomb-group (PcG) mutant phenotypes and show that it arose from the second, DNA binding component of Harbinger transposases. Molecular analysis of PcG compromised backgrounds reveals that ALP genes oppose silencing and H3K27me3 deposition at key PcG target genes. Proteomic analysis reveals that ALP1 and ALP2 are components of a variant PRC2 complex that contains the four core components but lacks plantspecific accessory components such as the H3K27me3 reader LIKE HETEROCHROMA-TION PROTEIN 1 (LHP1). We show that the N-terminus of ALP2 interacts directly with ALP1, whereas the C-terminus of ALP2 interacts with MULTICOPY SUPPRESSOR OF

Flower development is one of the particularly wellestablished model systems for investigating the molecular and genetic mechanisms underlying organogenesis in plants. Over the past 30 years, this work has led to detailed insights into many of the cellular and developmental processes that occur during the formation of flowers. This progress was made possible especially by the identification and characterization of the floral organ identity factors, which specify the different floral organ types in a combinatorial manner. However, in recent years, the genes that act downstream of these master regulators have taken center stage because it has become increasingly clear that they execute many of the functions originally attributed to the floral organ identity factors. In this Update, we will summarize and discuss our current view of floral organogenesis with particular emphasis on recent progress in the field (see "Advances" box). We will briefly describe the latest models for floral organ identity factor function and outline open questions that need to be addressed to better understand how they act at the mechanistic level. Furthermore, we will discuss studies that have begun to reveal how a complex interplay of transcription factors, hormones, regulatory RNAs, and epigenetic modifiers controls different developmental processes during the formation of flowers. Last, we will outline recent efforts to better understand the evolution of flowers and venture a look ahead at likely future developments in the field of flowering research.

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