Growing at the limit: Reef growth sensitivity to climate and oceanographic changes in the South Western Atlantic

This is the author accepted manuscript. The final version is available from Elsevier via the DOI in this recordWhilst the impacts of climatic and oceanographic change on lower latitude reefs are increasingly well documented, our understanding of how reef-building has fluctuated in higher latitude settings remains limited. Here, we explore the timing and longevity of reef-building through the mid- to late Holocene in the most southerly known reef (24°S) in the Western Atlantic. Reef core data show that reef growth was driven by a single coral species, Madracis decactis, and occurred over two phases since ~6000 calibrated (cal.) yr B.P.. These records further indicate that there was a clear growth hiatus from ~5500 to 2500 cal. yr B.P., and that there is no evidence of reef accretion on the Queimada Grande Reef (QGR) over the past 2000 yrs. It thus presently exists as a submerged senescent structure colonized largely by non-reef building organisms. Integration of these growth data with those from sites further north (18°S and 21°S) suggests that Intertropical Convergence Zone (ITCZ), South Westerlies Winds (SWW) and El Niño-Southern Oscillation (ENSO) variability and shifts during the Holocene drove changes in the position of the Brazil-Falklands/Malvinas Confluence (BFMC), and that this has had a strong regional influence on the timing and longevity of reef growth. Our results add new evidence to the idea that reef growth in marginal settings can rapidly turn-on or -off according to regional environmental changes, and thus are of relevance for predicting high latitude reef growth potential under climate change.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)razilian Research Council (CNPq

Regulated Nuclear Trafficking of rpL10A Mediated by NIK1 Represents a Defense Strategy of Plant Cells against Virus

The NSP-interacting kinase (NIK) receptor-mediated defense pathway has been identified recently as a virulence target of the geminivirus nuclear shuttle protein (NSP). However, the NIK1–NSP interaction does not fit into the elicitor–receptor model of resistance, and hence the molecular mechanism that links this antiviral response to receptor activation remains obscure. Here, we identified a ribosomal protein, rpL10A, as a specific partner and substrate of NIK1 that functions as an immediate downstream effector of NIK1-mediated response. Phosphorylation of cytosolic rpL10A by NIK1 redirects the protein to the nucleus where it may act to modulate viral infection. While ectopic expression of normal NIK1 or a hyperactive NIK1 mutant promotes the accumulation of phosphorylated rpL10A within the nuclei, an inactive NIK1 mutant fails to redirect the protein to the nuclei of co-transfected cells. Likewise, a mutant rpL10A defective for NIK1 phosphorylation is not redirected to the nucleus. Furthermore, loss of rpL10A function enhances susceptibility to geminivirus infection, resembling the phenotype of nik1 null alleles. We also provide evidence that geminivirus infection directly interferes with NIK1-mediated nuclear relocalization of rpL10A as a counterdefensive measure. However, the NIK1-mediated defense signaling neither activates RNA silencing nor promotes a hypersensitive response but inhibits plant growth and development. Although the virulence function of the particular geminivirus NSP studied here overcomes this layer of defense in Arabidopsis, the NIK1-mediated signaling response may be involved in restricting the host range of other viruses