2024-03-29T15:23:30Zhttp://digital.lib.washington.edu/dspace-oai/requestoai:digital.lib.washington.edu:1773/157672016-02-14T11:38:18Zcom_1773_15612com_1773_3774col_1773_15613
ResearchWorks
author
Jordan, Katherine C.
author
Schaeffer, Valerie
author
Fischer, Karin A.
author
Gray. Elizabeth E.
author
Ruohola-Baker, Hannele
2010-04-21T15:55:09Z
2010-04-21T15:55:09Z
2006-03-16
Jordan K, Schaeffer V, Fischer K, Gray E, Ruohola-Baker H. Notch signaling through Tramtrack bypasses the mitosis promoting activity of the JNK pathway in the mitotic-to-endocycle transition of Drosophila follicle cells. BMC Developmental Biology. 2006;6(1):16.
10.1186/1471-213X-6-16
http://www.biomedcentral.com/1471-213X/6/16
Background: The follicle cells of the Drosophila egg chamber provide an excellent model in which
to study modulation of the cell cycle. During mid-oogenesis, the follicle cells undergo a variation of
the cell cycle, endocycle, in which the cells replicate their DNA, but do not go through mitosis.
Previously, we showed that Notch signaling is required for the mitotic-to-endocycle transition,
through downregulating String/Cdc25, and Dacapo/p21 and upregulating Fizzy-related/Cdh1.
Results: In this paper, we show that Notch signaling is modulated by Shaggy and temporally
induced by the ligand Delta, at the mitotic-to-endocycle transition. In addition, a downstream target
of Notch, tramtrack, acts at the mitotic-to-endocycle transition. We also demonstrate that the JNK
pathway is required to promote mitosis prior to the transition, independent of the cell cycle
components acted on by the Notch pathway.
Conclusion: This work reveals new insights into the regulation of Notch-dependent mitotic-toendocycle
switch.
en_US
Notch signaling through Tramtrack bypasses the mitosis promoting activity of the JNK pathway in the mitotic-to-endocycle transition of Drosophila follicle cells
URL
https://digital.lib.washington.edu:443/researchworks/bitstream/1773/15767/1/1471-213X-6-16.pdf
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oai:digital.lib.washington.edu:1773/157692016-02-14T11:38:20Zcom_1773_15612com_1773_3774col_1773_15613
ResearchWorks
author
Smith, Erica D.
author
Kaeberlein, Tammi L.
author
Lydum, Brynn T.
author
Sager, Jennifer
author
Welton, K. Linnea
author
Kennedy, Brian K.
author
Kaeberlein, Matt
2010-04-21T15:55:21Z
2010-04-21T15:55:21Z
2008-05-05
Smith E, Kaeberlein T, Lydum B, et al. Age- and calorie-independent life span extension from dietary restriction by bacterial deprivation in Caenorhabditis elegans. BMC Developmental Biology. 2008;8(1):49.
10.1186/1471-213X-8-49
http://www.biomedcentral.com/1471-213X/8/49
Background: Dietary restriction (DR) increases life span and delays age-associated disease in many organisms. The mechanism by which DR enhances longevity is not well understood.
Results: Using bacterial food deprivation as a means of DR in C. elegans, we show that transient DR confers long-term benefits including stress resistance and increased longevity. Consistent with
studies in the fruit fly and in mice, we demonstrate that DR also enhances survival when initiated late in life. DR by bacterial food deprivation significantly increases life span in worms when initiated as late as 24 days of adulthood, an age at which greater than 50% of the cohort have died. These survival benefits are, at least partially, independent of food consumption, as control fed animals are
no longer consuming bacterial food at this advanced age. Animals separated from the bacterial lawn by a barrier of solid agar have a life span intermediate between control fed and food restricted animals. Thus, we find that life span extension from bacterial deprivation can be partially suppressed by a diffusible component of the bacterial food source, suggesting a calorie-independent mechanism for life span extension by dietary restriction.
Conclusion: Based on these findings, we propose that dietary restriction by bacterial deprivation increases longevity in C. elegans by a combination of reduced food consumption and decreased food
sensing.
en_US
Age- and calorie-independent life span extension from dietary
restriction by bacterial deprivation in Caenorhabditis elegans
URL
https://digital.lib.washington.edu:443/researchworks/bitstream/1773/15769/1/1471-213X-8-49.pdf
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https://digital.lib.washington.edu:443/researchworks/bitstream/1773/15769/2/1471-213X-8-49.pdf.txt
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oai:digital.lib.washington.edu:1773/158132016-02-14T11:39:01Zcom_1773_15612com_1773_3774col_1773_15613
ResearchWorks
author
Perez, Francisco A.
author
Curtis, Wendy R.
author
Palmiter, Richard D.
2010-05-06T20:02:37Z
2010-05-06T20:02:37Z
2005
Perez F, Curtis W, Palmiter R. Parkin-deficient mice are not more sensitive to 6-hydroxydopamine or methamphetamine neurotoxicity. BMC Neuroscience. 2005;6(1):71.
10.1186/1471-2202-6-71
http://www.biomedcentral.com/1471-2202/6/71
Background: Autosomal recessive juvenile parkinsonism (AR-JP) is caused by mutations in the parkin gene which encodes an E3 ubiquitin-protein ligase. Parkin is thought to be critical for
protecting dopaminergic neurons from toxic insults by targeting misfolded or oxidatively damaged proteins for proteasomal degradation. Surprisingly, mice with targeted deletions of parkin do not recapitulate robust behavioral or pathological signs of parkinsonism. Since Parkin is thought to protect against neurotoxic insults, we hypothesized that the reason Parkin-deficient mice do not
develop parkinsonism is because they are not exposed to appropriate environmental triggers. To test this possibility, we challenged Parkin-deficient mice with neurotoxic regimens of either
methamphetamine (METH) or 6-hydroxydopamine (6-OHDA). Because Parkin function has been linked to many of the pathways involved in METH and 6-OHDA toxicity, we predicted that Parkindeficient mice would be more sensitive to the neurotoxic effects of these agents.
Results: We found no signs consistent with oxidative stress, ubiquitin dysfunction, or
degeneration of striatal dopamine neuron terminals in aged Parkin-deficient mice. Moreover, results from behavioral, neurochemical, and immunoblot analyses indicate that Parkin-deficient mice are not more sensitive to dopaminergic neurotoxicity following treatment with METH or 6-OHDA.
Conclusion: Our results suggest that the absence of a robust parkinsonian phenotype in Parkindeficient
mice is not due to the lack of exposure to environmental triggers with mechanisms of action similar to METH or 6-OHDA. Nevertheless, Parkin-deficient mice could be more sensitive to other neurotoxins, such as rotenone or MPTP, which have different mechanisms of action;
therefore, identifying conditions that precipitate parkinsonism specifically in Parkin-deficient mice would increase the utility of this model and could provide insight into the mechanism of AR-JP.
Alternatively, it remains possible that the absence of parkinsonism in Parkin-deficient mice could reflect fundamental differences between the function of human and mouse Parkin, or the existence
of a redundant E3 ubiquitin-protein ligase in mouse that is not found in humans. Therefore, additional studies are necessary to understand why Parkin-deficient mice do not display robust
signs of parkinsonism.
en_US
Parkin-deficient mice are not more sensitive to 6-hydroxydopamine or methamphetamine neurotoxicity
Article
URL
https://digital.lib.washington.edu:443/researchworks/bitstream/1773/15813/1/1471-2202-6-71.pdf
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oai:digital.lib.washington.edu:1773/463002020-10-22T23:41:50Zcom_1773_15612com_1773_3774col_1773_15613
ResearchWorks
author
Giarmarco, Michelle
2020-10-22T23:41:49Z
2020-10-22T23:41:49Z
2020-10-15
http://hdl.handle.net/1773/46300
Cone photoreceptors in the retina are exposed to intense daylight, and have higher energy demands in darkness. Cones produce energy using a large cluster of mitochondria. Mitochondria are susceptible to oxidative damage, and healthy mitochondrial populations are maintained by regular turnover. Daily cycles of light exposure and energy consumption suggest that mitochondrial turnover is important for cone health. We investigated the 3-D ultrastructure and metabolic function of zebrafish cone mitochondria throughout the day. At night retinas undergo a mitochondrial biogenesis event, corresponding to an increase in the number of smaller, simpler mitochondria and increased metabolic activity in cones. In the daytime, ER and autophagosomes associate more with mitochondria, and mitochondrial size distribution across the cluster changes. We also report dense material shared between cone mitochondria that is extruded from the cell at night, sometimes forming extracellular structures. Our findings reveal an elaborate set of daily changes to cone mitochondrial structure and function.
CC0 1.0 Universal
Raw Data for "Daily Mitochondrial Mitochondrial Dynamics in Cone Photoreceptors"
Dataset
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URL
https://digital.lib.washington.edu:443/researchworks/bitstream/1773/46300/1/Giarmarco_PNAS_2020_rawdata%20-%20Michelle%20Giamarco.zip
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