Genetic composition and origin of juvenile green turtles foraging at Culebra, Puerto Rico, as revealed by mtDNA

Marine migratory species encounter a range of threats as they move through coastal and oceanic zones. Understanding the connectivity and dispersal patterns of such species is critical to their effective conservation. Here we analyzed the temporal genetic composition and the most likely origin of juvenile green turtles foraging at Puerto Manglar and Tortuga Bay, Culebra, Puerto Rico, using mitochondrial DNA control region sequences. We identified 17 haplotypes, of which CM-A3 (51.5%), CM-A5 (19.4%) and CM-A1 (13.6%) were the most common. Haplotype (h) and nucleotide (π) diversities were 0.680 and 0.008, respectively. There was no evidence of significant variation in the genetic composition of these aggregations throughout seven years (2000-2006), suggesting that relative contributions from source populations did not significantly change during this period. Mixed Stock Analysis (MSA), incorporating 14 Atlantic nesting populations as possible sources, indicated four main contributing stocks to the Culebra foraging grounds: Costa Rica (34.9%), Mexico (29.2%), East Central Florida (13.2%), and Suriname (12.0%). The regional pattern of connectivity among Wider Caribbean rookeries and Culebra was further evidenced by a second MSA using Atlantic Regional Management Units (RMUs) as sources, with 94.1% of the mixed stock attributed to this area. This study addresses the information gap on the connectivity of the green turtle in the North Atlantic, and establishes an important baseline that can be used to determine future changes in stock composition.Department of Natural and Environ-mental Resources of Puerto Rico; US National Marine Fisheries Service (NMFS-NOAA, Section 6, grant NA08NMF4720436); US Fish and Wildlife Service, Chelonia Inc, and WIDECAST. Work was conducted under permits by NMFS-NOAA (permit nos. 1253, 1518, 14949) and DNER (06-EPE-016). ARP had the support of the Portuguese Foundation for Science and Technologyinfo:eu-repo/semantics/publishedVersio

Profound reprogramming towards stemness in pancreatic cancer cells as adaptation to AKT inhibition

Cancer cells acquire resistance to cytotoxic therapies targeting major survival pathways by adapting their metabolism. The AKT pathway is a major regulator of human pancreatic adenocarcinoma progression and a key pharmacological target. The mechanisms of adaptation to long-term silencing of AKT isoforms of human and mouse pancreatic adenocarcinoma cancer cells were studied. Following silencing, cancer cells remained quiescent for long periods of time, after which they recovered proliferative capacities. Adaptation caused profound proteomic changes largely affecting mitochondrial biogenesis, energy metabolism and acquisition of a number of distinct cancer stem cell (CSC) characteristics depending on the AKT isoform that was silenced. The adaptation to AKT1 silencing drove most de-differentiation and acquisition of stemness through C-MYC down-modulation and NANOG upregulation, which were required for survival of adapted CSCs. The changes associated to adaptation sensitized cancer cells to inhibitors targeting regulators of oxidative respiration and mitochondrial biogenesis. In vivo pharmacological co-inhibition of AKT and mitochondrial metabolism effectively controlled pancreatic adenocarcinoma growth in pre-clinical models