In most flowering plants, a single megaspore mother cell (MMC) is differentiated from a pool of sporophytic cells in the distal ovule. Cai et al. show that a BR hormone gradient is generated in the distal nucellus of ovule primordia with a concave point in the MMC that is essential to restrict female germline fate to a single sub-epidermal cell.

Inflorescence architecture critically influences plant reproductive success and crop yield, and it reflects the activity of the inflorescence meristem and pedicel length. In Arabidopsis thaliana, the ERECTA (ER) signaling pathway and the SWR1 chromatin remodeling complex jointly regulate inflorescence architecture by promoting the expression of the PACLOBUTRAZOL RESISTANCE (PRE) gene family. However, how PREs regulate inflorescence architecture remains unclear. RNA-sequencing and chromatin immunoprecipitation coupled with quantitative PCR analyses were performed. Genetic interactions between HOMOLOG OF BEE2 INTERACTING WITH IBH1 (HBI1) and the SWR1-ER-MPK6 pathway in the control of inflorescence architecture were further studied. The present findings support that HBI1 functions downstream of PREs in the SWR1 and ER pathways to regulate inflorescence architecture by promoting pedicel elongation. Specifically, it binds to the promoters of the brassinosteroid (BR) biosynthesis gene CYP85A2 and a series of auxin-related genes, including auxin response factor ARF3, and promotes their expression. In turn, ARF3 can also bind to auxin signaling genes as well as CYP85A2 to activate their expression and promote pedicel elongation. Our study provides evidence that inflorescence architecture regulation by SWR1 and ER involves the HBI1 regulatory hub and its activation of both the BR and auxin hormone pathways.

Summary The signaling pathway mediated by the receptor‐like kinase ERECTA (ER) plays important roles in plant immune responses, but the underlying mechanism is unclear. Genetic interactions between ER signaling and the chromatin remodeling complex SWR1 in the control of plant immune responses were studied. Electrophoretic mobility shift assay and yeast one‐hybrid analysis were applied to identify ER‐WRKY33 downstream components. Chromatin immunoprecipitation analyses were further investigated. In this study, we show that the chromatin remodeling complex SWR1 enhances resistance to the white mold fungus Sclerotinia sclerotiorum in Arabidopsis thaliana via a process mediated by ER signaling. We identify a series of WRKY33 target YODA DOWNSTREAM (YDD) genes and demonstrate that SWR1 and ER signaling are required to enrich H2A.Z histone variant and H3K4me3 histone modification at YDDs and the binding of WRKY33 to YDD promoters upon S. sclerotiorum infection. We also reveal that the binding of WRKY33 to YDD promoters in turn promotes the enrichment of H2A.Z and H3K4me3 at YDD genes, thereby forming a positive regulatory loop to activate YDDs expression. Our study reveals how H2A.Z, H3K4me3 and ER signaling mutually regulate YDDs gene expression upon pathogen infection, highlighting the critical role of chromatin structure in ER‐signaling‐mediated plant immune responses.

Background: Calcium-dependent protein kinase (CPK) is one of the main Ca 2+ combined protein kinase that play significant roles in plant growth, development and response to multiple stresses. Despite an important member of the stress responsive gene family, little is known about the evolutionary history and expression patterns of CPK genes in pineapple. Results: Herein, we identified and characterized 17 AcoCPK genes from pineapple genome, which were unevenly distributed across eight chromosomes. Based on the gene structure and phylogenetic tree analyses, AcoCPKs were divided into four groups with conserved domain. Synteny analysis identified 7 segmental duplication events of AcoCPKs and 5 syntenic blocks of CPK genes between pineapple and Arabidopsis, and 8 between pineapple and rice. Expression pattern of different tissues and development stages suggested that several genes are involved in the functional development of plants. Different expression levels under various abiotic stresses also indicated that the CPK family underwent functional divergence during long-term evolution. AcoCPK1, AcoCPK3 and AcoCPK6, which were repressed by the abiotic stresses, were shown to be function in regulating pathogen resistance. Conclusions: 17 AcoCPK genes from pineapple genome were identified. Our analyses provide an important foundation for understanding the potential roles of AcoCPKs in regulating pineapple response to biotic and abiotic stresses