Are Populations of Economically Important Bonefish and Queen Conch \u27Open\u27 or \u27Closed\u27 in the Northern Caribbean Basin?

Demographics of co-occurring species can often be diagnosed through population genomic analyses of single nucleotide polymorphisms (SNPs). These data can define population structure, gene flow, and candidate regions in the genome that potentially reflect local adaptations. They can also gauge whether populations are demographically “open” or “closed” (i.e., with global or local recruitment). We derived SNPs from double-digest restriction-site associated DNA (ddRAD) to test the demographics of commercially important bonefish Albula vulpes (N = 117) and queen conch Lobatus gigas (N = 60) from two northeast Caribbean Basin islands (Grand Bahama to the north and Eleuthera to the south). Specifically, we tested the hypothesis that the strong west-to-east current in the Great Bahama Canyon is a vicariant barrier separating the two islands. We conducted Bayesian assignment tests on putatively neutral (A. vulpes = 36,206 SNPs; L. gigas = 64,863) and highly differentiated outlier datasets (A. vulpes = 123 and 79 SNPs; L. gigas = 88 and 51, respectively). For bonefish, results diagnosed asymmetrical gene flow and north-south differentiation, as potentially driven by adult mobility and easterly currents. However, both analyses indicated genetic structure in conch, substantiating the vicariant hypothesis. These results provide templates for future research endeavors with these impacted species. Outlier loci, for example, can potentially place populations of each within a demographic continuum, rather than within a dichotomous “open/closed” framework, as well as diagnose “source” and “sink” populations, as herein. These methodologies can then be applied to co-distributed species with similar but less well-understood ecologies so as to evaluate basin-wide trends in connectivity and local adaptation

Deletion of PPAR-γ in immune cells enhances susceptibility to antiglomerular basement membrane disease

Activation of the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) has been shown to be immunoregulatory in autoimmune diseases by inhibiting production of a number of inflammatory mediators. We investigated whether PPAR-γ gene deletion in hematopoietic cells would alter disease pathogenesis in the antiglomerular basement membrane (anti-GBM) mouse model. PPAR-γ+/+ and PPAR-γ−/− mice were immunized with rabbit antimouse GBM antibodies and lipopolysaccharide and evaluated for two weeks. Although both the PPAR-γ+/+ and PPAR-γ−/− mice had IgG deposition in the glomerulus and showed proteinuria two weeks after injection, glomerular and tubulointerstitial disease in PPAR-γ−/− mice were significantly more severe compared with the PPAR-γ+/+ animals. We observed that the PPAR-γ−/− mice had decreased CD4+CD25+ regulatory T cells and an increased CD8+:CD4+ ratio as compared with the PPAR-γ+/+ mice, suggesting that PPAR-γ has a role in the regulation of T cells. Furthermore, plasma interleukin-6 levels were significantly increased in the PPAR-γ−/− mice at two weeks as compared with the PPAR-γ+/+ animals. Taken together, these studies show that the lack of PPAR-γ expression enhances inflammatory renal disease in the anti-GBM antibody-induced glomerulonephritis mouse model and suggests targeting PPAR-γ may have therapeutic efficacy

Cdc14 phosphatase promotes segregation of telomeres through repression of RNA polymerase II transcription

Kinases and phosphatases regulate messenger RNA synthesis through post-translational modification of the carboxy-terminal domain (CTD) of the largest subunit of RNA polymerase II (ref. 1). In yeast, the phosphatase Cdc14 is required for mitotic exit2,3 and for segregation of repetitive regions4. Cdc14 is also a subunit of the silencing complex RENT (refs 5, 6), but no roles in transcriptional repression have been described. Here we report that inactivation of Cdc14 causes silencing defects at the intergenic spacer sequences of ribosomal genes during interphase and at Y′ repeats in subtelomeric regions during mitosis. We show that the role of Cdc14 in silencing is independent of the RENT deacetylase subunit Sir2. Instead, Cdc14 acts directly on RNA polymerase II by targeting CTD phosphorylation at Ser 2 and Ser 5. We also find that the role of Cdc14 as a CTD phosphatase is conserved in humans. Finally, telomere segregation defects in cdc14 mutants4 correlate with the presence of subtelomeric Y′ elements and can be rescued by transcriptional inhibition of RNA polymerase II