Figure 1. ARP4 and ARP6 in the regulation of flowering time.
a. Twenty-day-old wild type (WT) and ARP4 RNAi (ARP4-Ri) lines grown in long days. b. Sixty eight-day-old WT and ARP4-Ri plants grown under short day conditions.
c. Twenty-day-old wild type (WT) and arp6-1 plants grown in long days. d. Fifty-day-old WT and arp6-1 plants grown under short day conditions.
e. Major pathways controlling flowering time in Arabidopsis are summarized in this model abstracted from He and Amasino [69]. Gene activation is indicated by lines with arrowheads and repression is indicated by lines with bars. The MADS domain-containing transcription factor FLC (rectangular box) is a central repressor of the flowering program and acts to negatively regulate the expression of the transcription factors SOC1 and FT. In the absence of repression by FLC, SOC1 and FT promote the expression of AP1 and LFY, which serve to initiate the transition to flowering. Several pathways alter the activity of this central regulatory module either by their effects on FLC or its downstream target genes. The autonomous and vernalization pathways act to repress FLC expression and promote flowering under appropriate conditions, while FRI serves to upregulate FLC expression and inhibit flowering in the absence of an extended cold period. Under long day conditions, the photoperiod pathway upregulates the expression of FT and SOC1 via the transcription factor CO, promoting flowering. This pathway is also regulated by PHYB, and genetic data suggest that ARP4 also acts in or regulates the photoperiod pathway. In addition, gibberellin signaling pathways (GA) can also activate SOC1 and LFY, contributing to the transition to flowering. FRIGIDA (FRI) is a plant specific protein that signals long term cold exposure to FLC. The PAF1 complex, which appears to be homologous to the yeast complex of the same name, promotes FLC expression through histone methylation. Genetic and biochemical data suggest that ARP6 functions in a complex similar to yeast SWR1, and promotes FLC expression through deposition of the histone variant H2A.Z.
f. A model for maintenance of the vegetative phase of growth by the SWR1-like complex and its predicted ARP6, PIE1, and SEF subunits. The FLC gene is shown on the left in the transcriptionally activated or poised state and on the right in an inactive state in the arp6-1 mutant. Nucleosomes are shown as circles containing either histone H2A or the variant H2A.Z. Gene activation is indicated by arrows and gene repression is indicated by lines with bars. In the transcriptionally active state, H2A.Z, deposited by the SWR1-like complex facilitates the effects of various activator proteins. In this state the FLC protein is produced in abundance and it represses expression of the flowering-inducing genes FT and SOC1, thus maintaining the vegetative growth state. In the absence of H2A.Z deposition activity in arp6 and pie1 mutants, H2A.Z is not deposited into FLC chromatin and the gene remains permanently in a state incompetent for activation, resulting in early flowering in each generation. Under these conditions the FLC protein is not produced at high levels and its target genes FT and SOC1 become active. The FT and SOC1 proteins activate the floral-meristem identity genes AP1 and LFY, which induce the switch to flowering.
