Summary: One of the mechanisms involved in chromatin remodelling is so‐called ‘histone replacement’. An example of such a mechanism is the substitution of canonical H2A histone by the histone variant H2A.Z. The ATP‐dependent chromatin remodelling complex SWR1 is responsible for this action in yeast. We have previously proposed the existence of an SWR1‐like complex in Arabidopsis by demonstrating genetic and physical interaction of the components SEF, ARP6 and PIE1, which are homologues of the yeast Swc6 and Arp6 proteins and the core ATPase Swr1, respectively. Here we show that histone variant H2A.Z, but not canonical H2A histone, interacts with PIE1. Plants mutated at loci HTA9 and HTA11 (two of the three Arabidopsis H2A.Z‐coding genes) displayed developmental abnormalities similar to those found in pie1, sef and arp6 plants, exemplified by an early‐flowering phenotype. Comparison of gene expression profiles revealed that 65% of the genes differentially regulated in hta9 hta11 plants were also mis‐regulated in pie1 plants. Detailed examination of the expression data indicated that the majority of mis‐regulated genes were related to salicylic acid‐dependent immunity. RT‐PCR and immunoblotting experiments confirmed constitutive expression of systemic acquired resistance (SAR) marker genes in pie1, hta9 hta11 and sef plants. Variations observed at the molecular level resulted in phenotypic alterations such as spontaneous cell death and enhanced resistance to the phytopathogenic bacteria Pseudomonas syringae pv. tomato. Thus, our results support the existence in Arabidopsis of an SWR1‐like chromatin remodelling complex that is functionally related to that described in yeast and human, and attribute to this complex a role in maintaining a repressive state of the SAR response.

Helix-loop-helix transcription factors of the Ebf/Olf1 family have previously been implicated in the control of neurogenesis in the central nervous system in both Xenopus laevis and the mouse, but their precise roles have remained unclear. We have characterised two family members in the chick, and have performed a functional analysis by gain- and loss-of-function experiments. This study revealed several specific roles for Ebf genes in the spinal cord and hindbrain regions of higher vertebrates, and enabled their precise positioning along the neurogenic cascade.

The SWR1/SRCAP complex is a chromatin-remodeling complex that has been shown to be involved in substitution of histone H2A by the histone variant H2A.Z in yeast (Saccharomyces cerevisiae) and animals. Here, we identify and characterize SERRATED LEAVES AND EARLY FLOWERING (SEF), an Arabidopsis (Arabidopsis thaliana) homolog of the yeast SWC6 protein, a conserved subunit of the SWR1/SRCAP complex. SEF loss-of-function mutants present a pleiotropic phenotype characterized by serrated leaves, frequent absence of inflorescence internodes, bushy aspect, and flowers with altered number and size of organs. sef plants flower earlier than wild-type plants both under inductive and noninductive photoperiods. This correlates with strong reduction of FLOWERING LOCUS C and MADS-AFFECTING FLOWERING4 transcript levels and up-regulation of FLOWERING LOCUS T and SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 gene expression. The sef phenotype is similar to that of the photoperiod-independent early flowering1 (pie1) and the actin-related protein 6 (arp6) mutants. PIE1 and ARP6 proteins are also homologs of SWR1/SRCAP complex subunits. Analysis of sef pie1 double mutants demonstrates genetic interaction between these two genes. We also show physical interactions between SEF, ARP6, and PIE1 proteins. Taken together, our data indicate that SEF, ARP6, and PIE1 might form a molecular complex in Arabidopsis related to the SWR1/SRCAP complex identified in other eukaryotes.

Summary: In the cyanobacterium Synechocystis sp. PCC 6803, genes for Ni²⁺, Co²⁺, and Zn²⁺ resistance are grouped in a 12 kb gene cluster. The nrsBACD operon is composed of four genes, which encode proteins involved in Ni²⁺ resistance. Upstream from nrsBACD, and in opposite orientation, a transcription unit formed by the two genes rppA and rppB has been reported previously to encode a two‐component signal transduction system involved in redox sensing. In this report, we demonstrate that rppA and rppB (here redesigned nrsR and nrsS respectively) control the Ni²⁺‐dependent induction of the nrsBACD operon and are involved in Ni²⁺ sensing. Thus, expression of the nrsBACD operon was not induced by Ni²⁺ in a nrsRS mutant strain. Furthermore, nrsRS mutant cells showed reduced tolerance to Ni²⁺. Whereas the nrsBACD operon is transcribed from two different promoters, one constitutive and the other dependent on the presence of Ni²⁺ in the medium, the nrsRS operon is transcribed from a single Ni²⁺‐inducible promoter. The nrsRS promoter is silent in a nrsRS mutant background suggesting that the system is autoregulated. Purified full length NrsR protein is unable to bind to the nrsBACD‐nrsRS intergenic region; however, an amino‐terminal truncated protein that contains the DNA binding domain of NrsR binds specifically to this region. Our nrsRS mutant, which carries a deletion of most of the nrsR gene and part of the nrsS gene, does not show redox imbalance or photosynthetic gene mis‐expression, contrasting with the previously reported nrsR mutant.