RESUMO
Climate-induced shifts in flowering phenology can disrupt pollinator-floral resource synchrony, especially in desert ecosystems where rainfall dictates both. However, baseline metrics to gauge pollinator health in the wild amidst rapid climate change are lacking. Our laboratory-based study establishes a baseline for pollinator physiological state by exploring how osmotic conditions influence survivorship in a desert hawkmoth pollinator, Manduca sexta. We sampled hemolymph osmolality from over 1000 lab-grown moths at 20 %, 50 %, and 80 % ambient humidity levels. Starved moths maintained healthy osmolality of 350-400 mmol/kg for 1-3 days after eclosion regardless of ambient humidity, but it sharply rose to 550 mmol/kg after 4-5 days in low and moderate humidity, and after 5 days in high humidity. Starved moths in low humidity conditions perished within 5 days, while those in high humidity survived twice as long. Moths fed synthetic Datura wrightii nectar, synthetic Agave palmeri nectar, or water, maintained osmolality within a healthy range of 350-400mmol/kg. The same was true for moths fed authentic floral nectars from Datura and Agave plants, although moths consumed more synthetic than authentic nectars, possibly due to non-sugar constituents. Simulating a 4-day mismatch between pollinator emergence and nectar availability, a single nectar meal osmotically rescued moths under dry ambient conditions. Our findings highlight hemolymph osmolality as a rapid and accurate biomarker distinguishing dehydrated from hydrated states in insect pollinators.
RESUMO
The patterns by which primary tumors spread to metastatic sites remain poorly understood. Here, we define patterns of metastatic seeding in prostate cancer (PCa) using a novel injection-based mouse model - EvoCaP (Evolution in Cancer of the Prostate), featuring aggressive metastatic cancer to bone, liver, lungs, and lymph nodes. To define migration histories between primary and metastatic sites, we used our EvoTraceR pipeline to track distinct tumor clones containing recordable barcodes. We detected widespread intratumoral heterogeneity from the primary tumor in metastatic seeding, with few clonal populations (CPs) instigating most migration. Metastasis-to-metastasis seeding was uncommon, as most cells remained confined within the tissue. Migration patterns in our model were congruent with human PCa seeding topologies. Our findings support the view of metastatic PCa as a systemic disease driven by waves of aggressive clones expanding their niche, infrequently overcoming constraints that otherwise keep them confined in the primary or metastatic site.
