Project description:Seamounts, often rising hundreds of metres above the surrounding seafloor, obstruct the flow of deep-ocean water. While the resultant entrainment of deep-water by seamounts is predicted from ocean circulation models, its empirical validation has been hampered by the large scale and slow rate of the interaction. To overcome these limitations we use the growth of planktonic bacteria to assess the interaction rate. The selected study site, Tropic Seamount, in the North-Eastern Atlantic represents the majority of isolated seamounts, which do not affect the surface ocean waters. We prove deep-water is entrained by the seamount by measuring 2.3 times higher bacterial concentrations in the seamount-associated or ‘sheath’ water than in deep-ocean water unaffected by seamounts. Genomic analyses of the dominant sheath-water bacteria confirm their planktonic origin, whilst proteomic analyses indicate their slow growth. According to our radiotracer experiments, the doubling time of sheath-water bacterioplankton is 1.5 years. Therefore, for bacterioplankton concentration to reach 2.3 times higher in the ambient seawater, the seamount would need to retain deep-ocean water for more than 3.5 years. We propose that turbulent mixing of the retained sheath-water could stimulate bacterioplankton growth by increasing the cell encounter rate with the ambient dissolved organic molecules. If some of these molecules chelate hydroxides of iron and manganese, bacterioplankton consumption of the organic chelators would result in precipitation of insoluble hydroxides. Hence precipitated hydroxides would form ferromanganese deposits as a result of the bacterioplankton-mediated deep-water seamount interaction.
Project description:Processing of Immunoglobulin heavy chain (IgH) mRNA is a paradigm for competition between splicing and polyadenylation. In plasma cells pre-mRNA is polyadenylated mainly at the promoter-proximal secretory site while B-cells utilize a cryptic 5’ splice site in the last secretory-specific exon; these are mutually exclusive events for all IgH pre-mRNAs. Transcription elongation factor ELL2, more abundant in plasma cells relative to B-cells, was down-modulated by overexpression of heterogenous ribonucleoprotein F, a condition which reduced production of secretory IgH mRNA. Transfection of B-cells with ELL2 and the IgH reporter showed an accelerated use of the secretory poly(A) site, positioned in competition with the splice to M1; a small interfering RNA to ELL2 reduced expression of IgH secretory mRNA. Co-transcription factors ELL1 and PC4 were ineffective at driving secretory-poly(A) site use. ELL2 had little effect on poly(A) site choice with reporters containing tandem-linked poly(A) sites. Shorter forms of ELL2 protein result from both internal initiation at M186 and protein processing. An alternative splicing reporter driven by IgH or non-Ig promoters revealed that ELL2 and its M186 initiated form were able to accelerate exon skipping. Therefore, ELL2 influences IgH pre-mRNA processing through facilitating skipping of the alternative splice to the membrane form.