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Poster Full Abstracts - Physiology and Aging
Poster board number is above title. The first author is the presenter
332
Center México, Facultad de Ciencias, UNAM, México.
Sexual differentiation is a key activity during the development of organisms. In a particular species, the proportion of individuals of either gender is
balanced. Some environmental pollutants act as endocrine disruptors by altering the hormonal signaling cascade involved in sexual differentiation (1). In
mammals, the action of endocrine disruptors as beta-estradiol lead to the feminization of males (2). Herbicides like Atrazine are endocrine disruptors on
birds, amphibians and mammals (3). Goal: In this work we propose an
in vivo
experimental strategy to evaluate the ability of pollutants to cause reprotoxic
damage. Methods. We used two species of flies:
D. melanogaster
(DME) and
D. mojavensis
(DMO). The gene cascade involved in DME sexual
differentiation has been reported. DMO, is a cactophlic fly widely used in studies of speciation (4). Upon emerging, the testes of BMD males are colorless
but become red when ripe, so no dissection is needed to count the number of gonads per male (2, 1 or 0 testis). The last third of larval development was
chose for the exposure to genotoxins (Exterpro
TM
, glyphosate). 15 successive dilutions were prepared which were administered in the food for a semi-
chronic exposure. Adult flies recovered were counted, sexed and mated as follows (t, treated flies; nt untreated flies): ntFxtM, tFxntM and tFxtM. For each
concentration were evaluated 15 families individually. Results and Discussion. Treatment toxicity was similar for DME and DMO flies. The amount of
progeny decreased in the lower and higher concentrations assayed being the effect stronger when the females or both parents were exposed (
p<0.05
). This
methodology allows the in vivo assessment of reprotoxic damage. It needs to broaden the type of disruptors assayed. Acknowledgments. To the UC San
Diego
Drosophila
Stock Center for biological material; to Estefania Arroyo, Fernanda Ramírez, Estefanía García for technical support.
752B
Drosophila melanogaster as a model system to study macrophage migration inhibitory factor (MIF).
Blanka Rogina
1
, Tahereh Ziafazeli
1
, Maria
Renna
2
, Danny Soares
2
, Cynthia Staber
3
, Richard Bucala
4
, George Kuchel
2
, Robert Reenan
3
. 1) Dept Gen & Dev Biol, Univ Connecticut Hlth Ctr,
Farmington, CT; 2) UConn Ctr Aging, Division of Geriatric Medicine, Univ Connecticut Hlth Ctr, Farmington, CT; 3) Dept Mol Biol, Cell Biol and
Biochemistry, Brown University, Providence, RI; 4) Dept Medicine, Yale Univ School of Medicine, New Haven, CT.
Increased inflammation is often associated with age-associated disorders such as Alzheimer’s disease, sarcopenia, and frailty. MIF is a proinflammatory
cytokine involved in variety of processes such as inflammation, glucose metabolism, and tumorigenesis. MIF counterbalances anti-inflamatory effect of
glucocorticoids by increasing the expression of cytokines such as TNF-a, IL-2, IL-6 and others. High levels of MIF were found in long-lived calorie
restricted, long-lived Snell dwarf and growth hormone receptor knockout mice (GHR-KO) suggesting that increased MIF levels may be beneficial. However,
MIF-knockout mice are long lived illustrating complex relationship between MIF levels and longevity. Here describe how different levels of MIF mRNA
affect stress resistance, longevity and metabolism by using
Drosophila melanogaster
as a model system. Fruit flies do not have MIF but have the ABC MIF
transporter, and other components of MIF pathways. We established 20 stable transgenic lines that contain
Tribolium mif
gene MIF1A or MIF1B. These
transgenic lines allow us to express MIF pan-neuronally, in fat bodies or in muscles by using tissue specific Gene-Switch drivers: ELAV, S
1
106 drivers, or
MHC respectively. Overexpression of MIF1B in head resulted in a small beneficial effect on fly longevity and stress resistance. However, overexpressing
MIF in fat bodies has negative effect on longevity and stress resistance of flies, illustrating complex relationship between the levels and tissue of MIF
mRNA expression. The preliminary data suggest that flies can be used to determine effects of ectopic expression of the MIF gene on fly intermediary
metabolism in aging and under stress conditions.
753C
Sexual dimorphism for water balance mechanisms in montane populations of Drosophila kikkawai.
Vineeta Sharma
1,2
, Ravi Parkash
1
, Bhawna Kalra
1
.
1) Genetics, Maharshi Dyanand,University, Rohtak, India; 2) Centre for Cellular and Molecular Biology,Uppal Road, Hyderabad,India.
Conservation of water is critical to the ecological success of Drosophila species living in the drier montane localities of the Western Himalayas.We
observed clinal variation in desiccation resistance for both sexes of Drosophila kikkawai from an altitudinal transect (512-2226 (m).a.s.l.).Since more than
90 per cent of body water is lost through cuticular transpiration, the target of selection may be cuticular lipids or cuticular melanization. We tested whether
melanic females and non-melanic males of D. kikkawai have similar mechanism of desiccation resistance.There is clinal variation in the amount of cuticular
lipids per fly in males, but not in females.In contrast, for females, elevational increase in melanization is positively correlated with desiccation resistance and
negatively with cuticular water loss, but there is no variation in the amount of cuticular lipids. Thus, sexual dimorphism for the mechanism of desiccation
resistance in D. kikkawai matches the water proofing role of body melanization as well as cuticular lipids.
754A
A Novel p38 MAPK/Mef2/MnSOD Regulatory Mechanism in Aging and Oxidative Stress.
Alysia D. Vrailas-Mortimer
1,2
, Subhabrata Sanyal
1,2
. 1) Cell
Biology, Emory University, Atlanta, GA; 2) Center for Behavioral Neuroscience, Atlanta, GA.
Oxidative stress has been associated with a variety of diseases including neurodegenerative disorders, inflammation, and cancer. To best understand the
pathophysiology underlying oxidative stress-dependent diseases, it is essential to delineate the pathways that regulate oxidative stress. One such pathway is
the p38 MAPK (p38K), which is activated in response to oxidative stress in mammals and has been linked to aging and neurodegenerative disorders.
Although p38K is a bona fide stress activated protein kinase, specific stress-related signaling pathways regulated by p38K remain poorly understood.
Similarly, while p38K has been linked to aging and neurodegenerative disorders, the presence of four p38K genes in the mammalian genome has
complicated mechanistic investigation of p38K in these processes. Therefore, we have utilized Drosophila, which has two p38K genes (p38Ka and p38Kb)
in order to explore the function of p38K, with particular emphasis on the regulation of stress and aging. Loss of p38K leads to decreased viability, increased
levels of endogenous oxidative stress, shortened lifespan, and age-related locomotor behavior deficits, which can be rescued by add back of wild type p38Kb
in muscle, but not neurons. Conversely, over-expression of p38K in the muscle extends lifespan and is protective against environment oxidizing agents such
as Paraquat. Furthermore, we have found that p38K regulates expression of the mitochondrially localized antioxidant enzyme, MnSOD (SOD2), with loss of
p38K leading to a 50% decrease in MnSOD protein levels. Furthermore, over-expression of MnSOD in the p38K mutant background rescues lifespan, while
inhibition of MnSOD abolishes p38K-mediated lifespan extension. Finally, we find that p38K regulation of MnSOD is mediated by the muscle specific
transcription factor Mef2 as inhibition of Mef2 leads to decreased MnSOD expression. These results suggest that p38K might regulate lifespan through the
transcription factor Mef2 by modulating a SOD2-dependent oxidative stress response pathway in flies.