Abscisic acid (ABA) and jasmonic acid (JA) both inhibit seed germination, but their interactions during this process remain elusive. Here, we report the identification of a 'SAPK10-bZIP72-AOC' pathway, through which ABA promotes JA biosynthesis to synergistically inhibit rice seed germination. Using biochemical interaction and phosphorylation assays, we show that SAPK10 exhibits autophosphorylation activity on the 177 th serine, which enables it to phosphorylate bZIP72 majorly on 71 st serine. The SAPK10-dependent phosphorylation enhances bZIP72 protein stability as well as the DNA-binding ability to the G-box cis-element of AOC promoter, thereby elevating the AOC transcription and the endogenous concentration of JA. Blocking of JA biosynthesis significantly alleviated the ABA sensitivity on seed germination, suggesting that ABA-imposed inhibition partially relied on the elevated concentration of JA. Our findings shed a novel insight into the molecular networks of ABA-JA synergistic interaction during rice seed germination.

Ligand-dependent corepressor LCoR was identified as a protein that interacts with the estrogen receptor ␣ (ER␣) ligand binding domain in a hormone-dependent manner. LCoR also interacts directly with histone deacetylase 3 (HDAC3) and HDAC6. Notably, HDAC6 has emerged as a marker of breast cancer prognosis. However, although HDAC3 is nuclear, HDAC6 is cytoplasmic in many cells. We found that HDAC6 is partially nuclear in estrogen-responsive MCF7 cells, colocalizes with LCoR, represses transactivation of estrogen-inducible reporter genes, and augments corepression by LCoR. In contrast, no repression was observed upon HDAC6 expression in COS7 cells, where it is exclusively cytoplasmic. LCoR binds to HDAC6 in vitro via a central domain, and repression by LCoR mutants lacking this domain was attenuated. Kinetic chromatin immunoprecipitation assays revealed hormone-dependent recruitment of LCoR to promoters of ER␣-induced target genes in synchrony with ER␣. HDAC6 was also recruited to these promoters, and repeat chromatin immunoprecipitation experiments confirmed the corecruitment of LCoR with ER␣ and with HDAC6. Remarkably, however, although we find evidence for corecruitment of LCoR and ER␣ on genes repressed by the receptor, LCoR and HDAC6 failed to coimmunoprecipitate, suggesting that they are part of distinct complexes on these genes. Although small interfering RNA-mediated knockdown of LCoR or HDAC6 augmented expression of an estrogen-sensitive reporter gene in MCF7 cells, unexpectedly their ablation led to reduced expression of some endogenous estrogen target genes. Taken together, these data establish that HDAC6 can function as a cofactor of LCoR but suggest that they may act in enhance expressing some target genes.Nuclear receptors are ligand-regulated transcription factors whose activities are controlled by a variety of lipophilic extracellular signals, including steroid and thyroid hormones, metabolites of vitamins A (retinoids) and D (1, 2). DNA-bound nuclear receptors regulate transcription by recruiting complexes of coregulatory proteins, classified as coactivators or corepressors depending on whether they act to stimulate or repress transcription (2-4). Many coactivators interact with receptors through signature LXXLL motifs, known as NR boxes, which are oriented within a hydrophobic pocket of agonist-bound receptor ligand binding domains (5). Several coactivators or their associated cofactors possess histone acetyltransferase activity, which essentially caps positively charged lysine residues and loosens their association with DNA, facilitating chromatin remodeling and subsequent access of the transcriptional machinery to promoters.Nuclear receptor corepressors NCoR 7 and SMRT were isolated as factors that interacted with hormone-free but not hormone-bound thyroid and retinoid receptors (6, 7). They bind to receptor ligand binding domains through extended LXXX-IXXX(L/I) motifs known as CoRNR boxes (8, 9) and recruit multiprotein complexes implicated in transcriptional repression and histone deacetylatio...

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[1] A nested grid ocean circulation modeling system is used to examine the circulation, dispersion, and hydrodynamic connectivity of surface waters on the Belizean shelf. The nested grid system consists of a coarse-resolution ($19 km) outer model of the western Caribbean Sea, an intermediate-resolution ($6 km) middle model of the southern Meso-American Barrier Reef System (MBRS), and a fine-resolution ($2 km) inner model of the Belizean shelf. The nested system is forced by climatological monthly mean surface forcing and integrated over 5 years. The near-surface circulation on the Belize shelf produced by the inner model is characterized by a strong and persistent northwestward flow as a direct influence of the Caribbean Current on the northwestern shelf and a weak and spatially variable flow on the inner and southern shelf. The monthly mean model currents are used to calculate retention and dispersion of conservative, near-surface particles carried by the ocean currents. The near-surface dispersion is relatively higher in areas seaward (east) of Lighthouse and Glovers Reef atolls and lower on the inner shelf, particularly within the Inner Channel and in the vicinity of South Water Cay. To examine hydrodynamic connectivity of reefs in the surface waters of the Belize shelf, we calculate upstream and downstream retention areas for coral reefs at Turneffe Islands and Glovers Reef atolls. The potential sources of passive, near-surface particle supply reaching these two reef atolls within 30 days include both the shallow waters surrounding the two sites, the deep waters between them, and the coastal waters of the Bay Islands (Honduras). The 30-day downstream retention areas of the Turneffe and Glovers Reef atolls cover the central and southern Belize shelf, respectively.

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