6 research outputs found
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 (Ï) 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
Sleep is required to consolidate odor memory and remodel olfactory synapses
Animals with complex nervous systems demand sleep for memory consolidation and synaptic remodeling. Here, we show that, although the Caenorhabditis elegans nervous system has a limited number of neurons, sleep is necessary for both processes. In addition, it is unclear if, in any system, sleep collaborates with experience to alter synapses between specific neurons and whether this ultimately affects behavior. C. elegans neurons have defined connections and well-described contributions to behavior. We show that spaced odor-training and post-training sleep induce long-term memory. Memory consolidation, but not acquisition, requires a pair of interneurons, the AIYs, which play a role in odor-seeking behavior. In worms that consolidate memory, both sleep and odor conditioning are required to diminish inhibitory synaptic connections between the AWC chemosensory neurons and the AIYs. Thus, we demonstrate in a living organism that sleep is required for events immediately after training that drive memory consolidation and alter synaptic structures
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
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