Management Implications of Molt Migration by the Atlantic Flyway Resident Population of Canada Geese, Branta canadensis

We used satellite-tracked transmitters in 2001 and 2003 to document the timing, location, and extent of molt migrations by female Canada Geese (Branta canadensis) affiliated with the Atlantic Flyway Resident Population (AFRP) of Canada Geese that breed in the temperate region of eastern North America. Twenty-seven adult females were captured during the nesting period in late May and fitted with a satellite transmitter mounted either on a plastic neck collar or backpack harness. Nests of 24 birds were destroyed late in incubation to prevent renesting and ensure nest failure; three females did not have nests. Twelve of the 27 birds (44%) made a northward migration to molt in northern Quebec, Canada: seven to the eastern coast of Hudson Bay (58°12'N, 76°60'W), three to lowland areas east of James Bay (53°30'N, 79°02'W), and two to interior locations south of Ungava Bay (55°54'N, 68°24'W). Molt migrants were present in northern Quebec from June to September, a period that coincides with breeding ground aerial surveys and banding operations conducted for Atlantic Population (AP) Canada Geese that breed in this same region of northern Quebec. With >1 million AFRP geese estimated in the Atlantic Flyway, the potential exists for substantial numbers of yearling, sub-adult, and nest-failed or non-breeding adults to molt migrate to northern breeding areas and bias efforts to survey and mark AP geese. Within AFRP breeding areas, many local flocks have reached nuisance levels. We hypothesized that by inducing molt migration in breeding adults, through destruction of nests late in incubation, we would lessen recruitment, reduce numbers of summer resident adults with young, and increase adult mortality from hunting. However, molt migration behavior was not uniform throughout our study area. Molt migrants were from rural areas in New York, Pennsylvania, and Vermont, whereas marked birds that did not make molt migrations were from more coastal regions of the flyway. The 14 birds that did not make a molt migration remained within 60 km of their banding site. A genetic comparison of these two groups revealed no detectable differences. We conclude that failure to undergo a molt migration is likely attributed to the historical origin of captive-reared birds of mixed subspecies that comprise AFRP flocks in the eastern regions of the flyway and the availability of quality local habitat, distinct from brood-rearing areas, for molting

HIF-1 Modulates Dietary Restriction-Mediated Lifespan Extension via IRE-1 in Caenorhabditis elegans

Dietary restriction (DR) extends lifespan in various species and also slows the onset of age-related diseases. Previous studies from flies and yeast have demonstrated that the target of rapamycin (TOR) pathway is essential for longevity phenotypes resulting from DR. TOR is a conserved protein kinase that regulates growth and metabolism in response to nutrients and growth factors. While some of the downstream targets of TOR have been implicated in regulating lifespan, it is still unclear whether additional targets of this pathway also modulate lifespan. It has been shown that the hypoxia inducible factor-1 (HIF-1) is one of the targets of the TOR pathway in mammalian cells. HIF-1 is a transcription factor complex that plays key roles in oxygen homeostasis, tumor formation, glucose metabolism, cell survival, and inflammatory response. Here, we describe a novel role for HIF-1 in modulating lifespan extension by DR in Caenorhabditis elegans. We find that HIF-1 deficiency results in extended lifespan, which overlaps with that by inhibition of the RSKS-1/S6 kinase, a key component of the TOR pathway. Using a modified DR method based on variation of bacterial food concentrations on solid agar plates, we find that HIF-1 modulates longevity in a nutrient-dependent manner. The hif-1 loss-of-function mutant extends lifespan under rich nutrient conditions but fails to show lifespan extension under DR. Conversely, a mutation in egl-9, which increases HIF-1 activity, diminishes the lifespan extension under DR. This deficiency is rescued by tissue-specific expression of egl-9 in specific neurons and muscles. Increased lifespan by hif-1 or DR is dependent on the endoplasmic reticulum (ER) stress regulator inositol-requiring protein-1 (IRE-1) and is associated with lower levels of ER stress. Therefore, our results demonstrate a tissue-specific role for HIF-1 in the lifespan extension by DR involving the IRE-1 ER stress pathway

Dynamic Chromatin Organization during Foregut Development Mediated by the Organ Selector Gene PHA-4/FoxA

Central regulators of cell fate, or selector genes, establish the identity of cells by direct regulation of large cohorts of genes. In Caenorhabditis elegans, foregut (or pharynx) identity relies on the FoxA transcription factor PHA-4, which activates different sets of target genes at various times and in diverse cellular environments. An outstanding question is how PHA-4 distinguishes between target genes for appropriate transcriptional control. We have used the Nuclear Spot Assay and GFP reporters to examine PHA-4 interactions with target promoters in living embryos and with single cell resolution. While PHA-4 was found throughout the digestive tract, binding and activation of pharyngeally expressed promoters was restricted to a subset of pharyngeal cells and excluded from the intestine. An RNAi screen of candidate nuclear factors identified emerin (emr-1) as a negative regulator of PHA-4 binding within the pharynx, but emr-1 did not modulate PHA-4 binding in the intestine. Upon promoter association, PHA-4 induced large-scale chromatin de-compaction, which, we hypothesize, may facilitate promoter access and productive transcription. Our results reveal two tiers of PHA-4 regulation. PHA-4 binding is prohibited in intestinal cells, preventing target gene expression in that organ. PHA-4 binding within the pharynx is limited by the nuclear lamina component EMR-1/emerin. The data suggest that association of PHA-4 with its targets is a regulated step that contributes to promoter selectivity during organ formation. We speculate that global re-organization of chromatin architecture upon PHA-4 binding promotes competence of pharyngeal gene transcription and, by extension, foregut development

Effectiveness of lithium chloride in reducing waterfowl nest predation

Master of ScienceEcology, Fisheries, and WildlifeUniversity of Michiganhttp://deepblue.lib.umich.edu/bitstream/2027.42/114052/1/39015003271692.pd

Population ecology of the dusky Canada goose (Branata candensis occidentalis Baird)

Adult dusky Canada geese (Branta canadensis occidentalis Baird) were banded with plastic neck bands and observed on the winter range during 1985-92. Annual survival rates of adult geese estimated from observation data ranged from 76% to 85%. A model of Canada goose population dynamics was developed to illustrate relationships between survival rates, harvest regulations, and recruitment parameters and to predict trends in population size. Model simulations using recent estimates of survival and recruitment indicated that without significant increases in recruitment, survival rates must remain at or above present levels for the dusky Canada goose population to maintain itself. Observations of geese banded with tarsal and neck bands were used to estimate within-year survival rates and rates of neck band loss during 1990-92. Average monthly survival was 97% and was not significantly different among harvest and nonharvest periods (X², P = 0.3882). Neck band retention rates were 100% and 98% the first and second year after banding, respectively, for male and female geese. Resighting probabilities for neck and tarsal bands were significantly lower for female than for male geese (X², P < 0.020). Midwinter population size was estimated using neck band observations and a capture-resighting model. Dusky Canada goose population estimates ranged from 12,400 to 19,800 during 1990-92. Population estimates generally agreed with the U.S. Fish and Wildlife Service midwinter inventory during this period. Subflocks of wintering dusky Canada geese were identified using a clustering algorithm and the number of weeks neck banded geese were observed in regions of the winter range. Over 65% of geese in subflocks affiliated with the northern and southern regions of the winter range were never observed outside their region of affiliation. Geese affiliated with the middle regions of the winter range exhibited greater movement, as most were seen at least once outside their region of affiliation. Although large groups could be identified based on regional use patterns, associations between group members could only be demonstrated for small groups of [less than or equal to] 10 geese and adult pairs

The Target of Rapamycin pathway antagonizes pha-4/FoxA to control development and aging

FoxA factors are critical regulators of embryonic development and postembryonic life, but little is know about the upstream pathways that modulate their activity. C. elegans pha-4 encodes a FoxA transcription factor that is required to establish the foregut in embryos and to control growth and longevity after birth. We previously identified the AAA+ ATPase homolog ruvb-1 as a potent suppressor of pha-4 mutations.; Here we show that ruvb-1 is a component of the Target of Rapamycin (TOR) pathway in C. elegans (CeTOR). Both ruvb-1 and let-363/TOR control nucleolar size and promote localization of box C/D snoRNPs to nucleoli, suggesting a role in rRNA maturation. Inactivation of let-363/TOR or ruvb-1 suppresses the lethality associated with reduced pha-4 activity. The CeTOR pathway controls protein homeostasis and also contributes to adult longevity. We find that pha-4 is required to extend adult lifespan in response to reduced CeTOR signaling. Mutations in the predicted CeTOR target rsks-1/S6 kinase or in ife-2/eIF4E also reduce protein biosynthesis and extend lifespan, but only rsks-1 mutations require pha-4 for adult longevity. In addition, rsks-1, but not ife-2, can suppress the larval lethality associated with pha-4 loss-of-function mutations.; The data suggest that pha-4 and the CeTOR pathway antagonize one another to regulate postembryonic development and adult longevity. We suggest a model in which nutrients promote TOR and S6 kinase signaling, which represses pha-4/FoxA, leading to a shorter lifespan. A similar regulatory hierarchy may function in other animals to modulate metabolism, longevity, or disease