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  • American Association for the Advancement of Science (AAAS)  (19)
  • 2010-2014  (19)
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  • American Association for the Advancement of Science (AAAS)  (19)
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  • 2010-2014  (19)
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  • 1
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    American Association for the Advancement of Science (AAAS) ; 2011
    In:  Science Signaling Vol. 4, No. 158 ( 2011-02)
    Details
    In: Science Signaling, American Association for the Advancement of Science (AAAS), Vol. 4, No. 158 ( 2011-02)
    Abstract: Circadian rhythms, which have a periodicity of ~24 hours, regulate many physiological and metabolic processes. From algae to humans, circadian rhythms are regulated by a transcription-translation feedback loop. The products of clock genes are transcriptional activators that drive the expression of repressor genes, whose products feed back to inhibit the activators (see Bass and Takahashi). O’Neill and Reddy investigated a role for nontranscriptional control of circadian rhythms in human red blood cells (RBCs), which lack nuclei and cannot support transcription. The authors monitored peroxiredoxins, proteins that protect RBCs from peroxides by becoming oxidized and forming dimers, which are then reduced to the monomeric form. The authors found that peroxiredoxins exhibited a circadian redox rhythm in RBCs kept in the dark at constant temperature. This cycle could be entrained by temperature and was not affected by inhibitors of transcription or translation. The equilibrium between dimeric hemoglobin (a source of peroxide) and tetrameric hemoglobin (which produces less peroxide) also exhibited a circadian rhythm, as did the reducing agents NADH and NADPH. The redox cycle of peroxiredoxins in mouse NIH 3T3 cells also exhibited a circadian rhythm, and this was altered in cells from mice deficient in clock genes. Conversely, knockdown of various peroxiredoxin-encoding genes in human cells had effects on circadian gene expression. In an accompanying study, O’Neill et al . examined circadian rhythms in the simple alga Ostreococcus tauri . When kept at constant temperature in the dark, circadian rhythms in the alga that are controlled by transcription-translation loops are suspended until it is reexposed to light. However, the cycles continue from the point at which darkness occurred, rather than becoming reset. The authors found that redox cycles of peroxiredoxins in the alga persisted in the dark in a transcription-independent manner and that inhibitors of clocks in mammalian cells had similar effects in the alga. Together, these studies suggest that nontranscriptional metabolic cycles couple with genetic oscillators to control rhythmic outputs. J. S. O’Neill, A. B. Reddy, Circadian clocks in human red blood cells. Nature 469 , 498–503 (2011). [Online Journal] J. S. O’Neill, G. van Ooijen, L. E. Dixon, C. Troein, F. Corellou, F.-Y. Bouget, A. B. Reddy, A. J. Millar, Circadian rhythms persist without transcription in a eukaryote. Nature 469 , 554–558 (2011). [Online Journal] J. Bass, J. S. Takahashi, Redox redux. Nature 469 , 476–478 (2011). [Online Journal]
    Type of Medium: Online Resource
    ISSN: 1945-0877 , 1937-9145
    URL: Article
    DOI: 10.1126/scisignal.4158ec29
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2011
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  • 2
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    Adjusting for Stochasticity?
    American Association for the Advancement of Science (AAAS) ; 2012
    In:  Science Signaling Vol. 5, No. 220 ( 2012-04-17)
    Details
    In: Science Signaling, American Association for the Advancement of Science (AAAS), Vol. 5, No. 220 ( 2012-04-17)
    Abstract: Reversible receptor methylation serves as the main mechanism enabling the rapid adaptation of bacterial chemotaxis machinery to allow directional movement through a gradient (see Hazelbauer). Yuan et al . describe a longer-acting mechanism, detectable in bacteria genetically deficient in the enzymes responsible for reversible receptor methylation, for adaptation of the bacterial chemotaxis machinery to changes in the concentration of the phosphorylated protein CheY-P, which binds to the flagellar motor protein FliM to trigger a change in the rotation of the motor. Receptor activation reduces the receptor’s kinase activity, which reduces the amount of CheY-P, causing the bacteria to switch from a tumbling movement when CheY-P is bound to FliM to a running, directional movement when FliM is not bound to CheY-P. Yuan et al. showed that cells defective in the receptor-level adaptation machinery exhibited partial adaptation to a chemoattractant stimulus, and mathematical modeling suggested that this may arise through a change in the abundance of FliM. The authors tested this prediction using total internal reflection fluorescence (TIRF) microscopy and fluorescent protein–tagged FliM and showed that the number of FliM molecules increased by ~25% in response to conditions that produced partial adaptation. This slow mechanism of adaptation does not contribute to the rapid adaptation observed in wild-type bacteria encountering a chemoattractant gradient but may match the motor proteins with intrinsic cell-cell differences in the output of the chemotaxis signaling machinery to ensure that stochastic differences among the cells do not compromise chemotaxis behavior. J. Yuan, R. W. Branch, B. G. Hosu, H. C. Berg, Adaptation at the output of the chemotaxis signalling pathway. Nature 484 , 233–236 (2012). [Online Journal] G. L. Hazelbauer, Adaptation by target remodelling. Nature 484 , 173–175 (2012). [Online Journal]
    Type of Medium: Online Resource
    ISSN: 1945-0877 , 1937-9145
    URL: Article
    DOI: 10.1126/scisignal.2003140
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2012
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  • 3
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    Attack of the Clones
    American Association for the Advancement of Science (AAAS) ; 2012
    In:  Science Vol. 337, No. 6095 ( 2012-08-10), p. 636-638
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 337, No. 6095 ( 2012-08-10), p. 636-638
    Abstract: Fungi have become a greater global threat to crops, forests, and wild animals than ever before. They have killed countless amphibians, pushing some species to extinction, and they're threatening the food supply for billions of people. A Nature paper, published in April to great interest, says the world isn't fully aware of the dangers and should invest more in countermeasures. Scientists around the world have sent in articles describing other fungal diseases that could have bolstered the paper. Among the wide variety of species under attack are crabs, corals, corn, and the Cavendish banana—and new fungal diseases are discovered every year. In June, Elsevier presented a new journal called Medical Mycology Case Reports , completely devoted to "unusual medical or veterinary fungal infections."
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.337.6095.636
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    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2012
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  • 4
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    What's killing the reindeer?
    American Association for the Advancement of Science (AAAS) ; 2014
    In:  Science Vol. 346, No. 6210 ( 2014-11-07), p. 685-685
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 346, No. 6210 ( 2014-11-07), p. 685-685
    Abstract: An ecologist's study of reindeer has touched off a firestorm. Each year, Sami herders in Norway file compensation claims for tens of thousands of reindeer deaths that they blame on carnivores, primarily lynx and wolverines. Ecologist Torkild Tveraa, however, pins the blame on overpopulation: The land simply cannot support the herds. Tveraa, who is with the Norwegian Institute for Nature Research in Tromsø, first presented his case in a government-funded report last year, and he added new analysis in a study published in the October issue of the Journal of Applied Ecology . The government has pointed to the findings as exonerating the threatened lynx and wolverines, which are already protected by strict hunting limits. To the Sami, however, the study threatens an economic lifeline.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.346.6210.685
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    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2014
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  • 5
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    The NADPH Survival Advantage
    American Association for the Advancement of Science (AAAS) ; 2012
    In:  Science Signaling Vol. 5, No. 227 ( 2012-06-05)
    Details
    In: Science Signaling, American Association for the Advancement of Science (AAAS), Vol. 5, No. 227 ( 2012-06-05)
    Abstract: Under conditions of metabolic stress that lead to a decrease in the intracellular concentration of adenosine triphosphate (ATP), liver kinase B1 (LKB1) is activated, which in turn phosphorylates and activates adenosine monophosphate (AMP)–activated protein kinase (AMPK), which modulates glucose metabolism and autophagy in the cell to promote energy homeostasis. The LKB1-AMPK signaling pathway is also activated in tumor cells in response to certain oncogenes and as a result of the detachment of cells from the extracellular matrix. Noting that cells deficient in LKB1 or AMPK are resistant to oncogenic transformation, Jeon et al . investigated how AMPK modulated metabolism in tumor cells. A549 cells, a human epithelial cancer cell line deficient in LKB1, were more sensitive than LKB1-sufficient cell lines to cell death induced by glucose deprivation. In addition, LKB1-deficient cells exhibited increased NADPH depletion and oxidative stress during glucose deprivation compared with LKB1-sufficient cells. NADPH is consumed by fatty acid synthesis (FAS) and generated through fatty acid oxidation (FAO). NAPDH reduces oxidative stress in cells by detoxifying hydrogen peroxide. AMPK phosphorylates and inhibits the enzymes acetyl-CoA carboxylase 1 (ACC1) and ACC2, thereby inhibiting FAS and increasing FAO. The authors found that knockdown of ACC1 or ACC2 substantially inhibited A549 cell death induced by glucose deprivation. Additionally, AMPK activation was required for the inhibition of the ACCs and for the maintenance of NAPDH abundance in cells during conditions of glucose deprivation or matrix detachment. Tumor growth in mice injected with oncogenic fibroblasts expressing mutant ACC isoforms that could not be phosphorylated by AMPK was reduced compared to that in mice injected with control tumor cells. Together, these data suggest that under conditions of metabolic stress, AMPK maintains NAPDH concentrations in tumor cells to reduce oxidative stress and promote survival. As Svensson and Shaw discuss in commentary, future work will determine how the timing and context of LKB1-AMPK signaling determine tumor cell survival. S.-M. Jeon, N. S. Chandel, N. Hay, AMPK regulates NAPDH homeostasis to promote tumour cell survival during energy stress. Nature 485 , 661–665 (2012). [Online Journal] R. U. Svensson, R. J. Shaw, Tumour friend or foe. Nature 485 , 590–591 (2012). [Online Journal]
    Type of Medium: Online Resource
    ISSN: 1945-0877 , 1937-9145
    URL: Article
    DOI: 10.1126/scisignal.2003284
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2012
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  • 6
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    A unified cause for adrenal Cushing's syndrome
    American Association for the Advancement of Science (AAAS) ; 2014
    In:  Science Vol. 344, No. 6186 ( 2014-05-23), p. 804-805
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 344, No. 6186 ( 2014-05-23), p. 804-805
    Abstract: In the cartoon adventure Falling Hare , aviator Bugs Bunny is vexed by a series of aerial mishaps, causing his airplane to crash. After spending the episode trying to understand the origin of his problem, Bugs hits on the obvious solution: a gremlin. Four papers—two on pages 913 and 917 in this issue of Science ( 1 , 2 ), a third in the New England Journal of Medicine ( 3 ), and a fourth in Nature Genetics ( 4 ), all from different groups—describe the use of whole exome sequencing (WES) to reach similar conclusions regarding the molecular origin of cortisol-producing adrenocortical adenomas. Just like Bugs' sudden recognition of the gremlin's underlying role in his predicament, the surprisingly consistent answer to the question of the underlying cause of these tumors is no longer obscure; rather, it is a mutation in the catalytic subunit of the signaling subunit of the cyclic-AMP (cAMP)–dependent protein kinase, protein kinase A (PKA).
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.1254901
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    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2014
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    detail.hit.zdb_id: 2066996-3
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  • 7
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    Life and Death with Salicylic Acid
    American Association for the Advancement of Science (AAAS) ; 2012
    In:  Science Signaling Vol. 5, No. 229 ( 2012-06-19)
    Details
    In: Science Signaling, American Association for the Advancement of Science (AAAS), Vol. 5, No. 229 ( 2012-06-19)
    Abstract: When a plant is attacked by a pathogen, effector-triggered immunity is induced, which results in programmed cell death (PCD) at the site of infection and systemic acquired resistance (SAR) in other areas of the plant. SAR depends on the hormone salicylic acid (SA), which is produced at the site of infection and gradually decreases in concentration with increasing distance from the site of infection (see commentary by Gust and Nürnberger). SA controls the nuclear translocation of the transcriptional cofactor nonexpresser of PR genes 1 (NPR1), which is required for SAR. When NPR1 is degraded, cells undergo PCD, whereas when NPR1 accumulates in the nucleus, it induces the expression of genes required for SAR. Noting that degradation of NPR1 acts as a molecular switch to determine the response to infection, Fu et al . sought binding partners of NPR1 that might regulate its targeting by the CUL3 E3 ubiquitin ligase system in Arabidopsis thaliana . They found that loss of the NPR1 homologs NPR3 or NPR4, which contain domains typical of CUL3 adaptor proteins, prevented CUL3-dependent degradation of NPR1. Yeast two-hybrid studies and pull-down assays showed that NPR3 and NPR4 individually interacted with NPR1; however, NPR3 interacted with NPR1 only in the presence of SA and NPR4 interacted with NPR1 only in the absence of SA. Binding studies with [ 3 H]-SA showed that NPR3 was a low-affinity receptor for SA, whereas NPR4 was a high-affinity receptor. Studies of wild-type or NPR3- or NPR4-mutant Arabidopsis infected with a pathogen showed that loss of either NPR3 or NPR4 had differential effects on plant responses. These data led the authors to propose a model in which SA, which is at high concentration at the site of infection, binds to NPR3, enabling it to recruit CUL3 to NPR1, which leads to NPR1 degradation and PCD. In contrast, at more distant sites, SA is lower in concentration and binds only to the high-affinity receptor NPR4, which blocks its interaction with NPR1, causing NPR1 to accumulate, translocate to the nucleus, and induce SAR. Z. Q. Fu, S. Yan, A. Saleh, W. Wang, J. Ruble, N. Oka, R. Mohan, S. H. Spoel, Y. Tada, N. Zheng, X. Dong, NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants. Nature 486 , 228–232 (2012). [Online Journal] A. D. Gust, T. Nürnberger, A life or death switch. Nature 486 , 198–199 (2012). [Online Journal]
    Type of Medium: Online Resource
    ISSN: 1945-0877 , 1937-9145
    URL: Article
    DOI: 10.1126/scisignal.2003315
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2012
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  • 8
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    Getting Choosy
    American Association for the Advancement of Science (AAAS) ; 2011
    In:  Science Signaling Vol. 4, No. 193 ( 2011-10-04)
    Details
    In: Science Signaling, American Association for the Advancement of Science (AAAS), Vol. 4, No. 193 ( 2011-10-04)
    Abstract: Members of the NOD-like receptor (NLR) family of cytosolic proteins respond to microbial components in the cytoplasm of infected cells by forming multiprotein complexes called inflammasomes, which stimulate the processing and activation of caspase 1. This protease then processes precursor forms of the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18, which induce cell death. NLRC4-containing inflammasomes are formed in response to the bacterial proteins flagellin and PrgJ, a conserved component of the type-III secretion system (TTSS); however, how NLRC4 responds to specific stimuli is unclear (see commentary by Monack). Two groups now implicate NLR family members called NAIPs (NLR family, apoptosis inhibitory proteins) in determining the ligand specificity of NLRC4 inflammasome activation. Kofoed and Vance showed that mouse macrophages lacking NAIP2 failed to activate caspase 1 or undergo cell death in response to PrgJ; however, loss of NAIP2 had no effect on cell death induced by flagellin. In contrast, NAIP5 was required for flagellin-induced caspase 1 activation but was not necessary for cell death induced by PrgJ. Experiments in a reconstituted in vitro system showed that stimulation of NLRC4 inflammasome formation by flagellin required NAIP5, and NAIP5 and flagellin were also present in the complex. In contrast, PrgJ did not induce NAIP5-NLRC4 inflammasome formation but did stimulate complex formation between NAIP2 and NLRC4. Zhao et al . also demonstrated the ability of NAIP2 and NAIP5 to activate NLRC4 inflammasome formation in mouse cells in response to distinct ligands from various bacteria. In addition, they showed that CprI (a TTSS component from Chromobacterium violaceum ), but not flagellin, activated NLRC4 inflammasome formation in a human macrophage cell line and that CprI bound to NAIP, the sole human NAIP protein. Together, these data suggest that NAIP proteins bind directly to distinct microbial products and confer ligand specificity to NLRC4 inflammasomes. E. M. Kofoed, R. E. Vance, Innate immune recognition of bacterial ligands by NAIPs determines inflammasome specificity. Nature 477 , 592–595 (2011). [PubMed] Y. Zhao, J. Yang, J. Shi, Y.-N. Gong, Q. Lu, H. Xu, L. Liu, F. Shao, The NLRC4 inflammasome receptors for bacterial flagellin and type III secretion apparatus. Nature 477 , 596–600 (2011). [PubMed] D. M. Monack, Recognition of a unique partner. Nature 477 , 543–544 (2011). [Online Journal]
    Type of Medium: Online Resource
    ISSN: 1945-0877 , 1937-9145
    URL: Article
    DOI: 10.1126/scisignal.4193ec274
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2011
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  • 9
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    Time to Metabolize
    American Association for the Advancement of Science (AAAS) ; 2012
    In:  Science Signaling Vol. 5, No. 205 ( 2012-01-03)
    Details
    In: Science Signaling, American Association for the Advancement of Science (AAAS), Vol. 5, No. 205 ( 2012-01-03)
    Abstract: Circadian clocks in peripheral organs are set by metabolic cues. Lamia et al. (see also the commentary by Bass) investigated whether circadian clocks regulate metabolism and found that the cryptochrome proteins Cry1 and Cry2, which are components of the circadian clock, interact with various nuclear hormone receptors, including the glucocorticoid receptor. The interaction of Cry1 with the glucocorticoid receptor was enhanced by the synthetic glucocorticoid dexamethasone and decreased the ability of the glucocorticoid receptor to transcriptionally activate a luciferase reporter gene. Compared with fibroblasts from wild-type mice, dexamethasone treatment of fibroblasts from mice deficient in both cytochromes ( cry1 –/– ;cry2 –/– ) decreased the number of genes that were transcriptionally repressed, increased the number of genes that were transcriptionally activated, and increased the extent of transcriptional activation of a specific target gene ( sgk1 , which encodes serum- and glucocorticoid-regulated kinase 1). At night, glucocorticoids are less effective at inducing the expression of pck1 , the gene encoding the gluconeogenic enzyme phosphoenolpyruvate carboxykinase 1, and the association of Cry1 and Cry2 with the glucocorticoid response element in the pck1 promoter increased at night after dexamethasone treatment. In addition, dexamethasone-triggered induction of pck1 expression was increased in livers from cry1 –/– ;cry2 –/– mice compared with those from wild-type mice. Long-term dexamethasone treatment suppressed production of endogenous corticosterone to a lesser extent in cry1 –/– ;cry2 –/– mice than in wild-type mice, which suggests a role for cryptochromes in the negative-feedback loop that suppresses glucocorticoid synthesis. Long-term dexamethasone treatment also triggered more pronounced fasting hyperglycemia and glucose intolerance in cry1 –/– ;cry2 –/– mice compared with wild-type mice. Thus, cryptochromes inhibit glucose metabolism by suppressing transcription through the glucocorticoid receptor. K. A. Lamia, S. J. Papp, R. T. Yu, G. D. Barish, N. H. Uhlenhaut, J. W. Jonker, M. Downes, R. M. Evans, Cryptochromes mediate rhythmic repression of the glucocorticoid receptor. Nature 480 , 552–556 (2011). [PubMed] J. Bass, On time metabolism. Nature 480 , 466-467 (2011). [Online Journal]
    Type of Medium: Online Resource
    ISSN: 1945-0877 , 1937-9145
    URL: Article
    DOI: 10.1126/scisignal.2002812
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2012
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  • 10
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    Food Fit for a Queen
    American Association for the Advancement of Science (AAAS) ; 2011
    In:  Science Signaling Vol. 4, No. 175 ( 2011-05-31)
    Details
    In: Science Signaling, American Association for the Advancement of Science (AAAS), Vol. 4, No. 175 ( 2011-05-31)
    Abstract: Royal jelly is a protein-, sugar-, lipid-, and mineral-containing food that is produced by worker bees of honeybee hives and that stimulates the development of a new queen bee (see Robinson for commentary). Kamakura noted that royal jelly lost its effectiveness after storage and isolated a protein, called royalactin, that was as effective as royal jelly in promoting the phenotypic changes associated with development of the queen—shortened developmental time, increased size of the adult, and increased ovary size. To explore the details of the pathways that might be responsible for these effects of royalactin, Kamakura fed royalactin to the fruit fly, Drosophila melanogaster , which does not have queens and workers, and found that the flies exhibited an increase in body weight and length, increased fecundity, and increased life span, which are all characteristics of the queen honeybee. Using flies with mutations or carrying RNA interference (RNAi) transgenes that disrupt various signaling pathways, Kamakura determined that royalactin signals through the epidermal growth factor receptor (EGFR) in the fat body. The effects on body size required EGFR-mediated signaling through PI3K-TOR-S6K (phosphatidylinositol 3-kinase to target of rapamycin to S6 kinase), a pathway known for stimulating protein synthesis and mediating growth. Activation of the mitogen-activated protein kinase (MAPK) pathway downstream of the EGFR was required for the shortened developmental time, and this was mediated by an increase in the production of the steroid hormone 20-hydroxyecdysone. EGFR signaling stimulated the production of juvenile hormone, transcription of the gene encoding yolk protein, and fecundity, but these effects were not affected by disruption of the MAPK or PI3K-TOR-S6K pathways, suggesting that there is another arm of EGFR signaling that functions in this process. How royalactin promotes longevity also remains an open question. Armed with this information from the fruit fly, Kamakura returned to the honeybee and showed by RNAi and selective pathway inhibition that EGFR and the pathways identified in the flies were involved in the increase in body size and shortening of developmental time associated with development of the honeybee queen in response to royalactin. M. Kamakura, Royalactin induces queen differentiation in honeybees. Nature 473 , 478–483 (2011). [PubMed] G. E. Robinson, Royal aspirations. Nature 473 , 454–455 (2011). [Online Journal]
    Type of Medium: Online Resource
    ISSN: 1945-0877 , 1937-9145
    URL: Article
    DOI: 10.1126/scisignal.4175ec151
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2011
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