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Neuronal IL-17 Controls C. elegans D...
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Godthi, Abhishiktha,
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Neuronal IL-17 Controls C. elegans Developmental Diapause Through CEP-1/p53 /
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Neuronal IL-17 Controls C. elegans Developmental Diapause Through CEP-1/p53 // Abhishiktha Godthi.
作者:
Godthi, Abhishiktha,
面頁冊數:
1 electronic resource (243 pages)
附註:
Source: Dissertations Abstracts International, Volume: 86-03, Section: B.
Contained By:
Dissertations Abstracts International86-03B.
標題:
Developmental biology. -
電子資源:
https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31332288
ISBN:
9798384031871
Neuronal IL-17 Controls C. elegans Developmental Diapause Through CEP-1/p53 /
Godthi, Abhishiktha,
Neuronal IL-17 Controls C. elegans Developmental Diapause Through CEP-1/p53 /
Abhishiktha Godthi. - 1 electronic resource (243 pages)
Source: Dissertations Abstracts International, Volume: 86-03, Section: B.
During metazoan development, how cell division and metabolic programs are coordinated with nutrient availability remains unclear. Here, we show that nutrient availability signaled by the neuronal cytokine, ILC-17.1 switches C. elegans development between reproductive growth and dormancy by controlling the activity of the tumor suppressor p53 ortholog, CEP-1. Specifically, upon food availability, ILC-17.1 signaling by amphid neurons promotes glucose utilization and suppresses CEP-1/p53 to allow growth. In the absence of ILC-17.1, CEP-1/p53 is activated, upregulates cell-cycle inhibitors, decreases phosphofructokinase and cytochrome C expression, and causes larvae to arrest as stress-resistant, quiescent dauers. We propose a model whereby ILC-17.1 signaling links nutrient availability and energy metabolism to cell cycle progression through CEP-1/p53. These studies describe ancestral functions of IL-17s and the p53-family of proteins and are relevant to our understanding of neuroimmune mechanisms in cancer. They also reveal a DNA damage-independent function of CEP-1/p53 in invertebrate development and support the existence of a previously undescribed C. elegans dauer pathway.
English
ISBN: 9798384031871Subjects--Topical Terms:
592588
Developmental biology.
Subjects--Index Terms:
Neuronal cytokine
Neuronal IL-17 Controls C. elegans Developmental Diapause Through CEP-1/p53 /
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During metazoan development, how cell division and metabolic programs are coordinated with nutrient availability remains unclear. Here, we show that nutrient availability signaled by the neuronal cytokine, ILC-17.1 switches C. elegans development between reproductive growth and dormancy by controlling the activity of the tumor suppressor p53 ortholog, CEP-1. Specifically, upon food availability, ILC-17.1 signaling by amphid neurons promotes glucose utilization and suppresses CEP-1/p53 to allow growth. In the absence of ILC-17.1, CEP-1/p53 is activated, upregulates cell-cycle inhibitors, decreases phosphofructokinase and cytochrome C expression, and causes larvae to arrest as stress-resistant, quiescent dauers. We propose a model whereby ILC-17.1 signaling links nutrient availability and energy metabolism to cell cycle progression through CEP-1/p53. These studies describe ancestral functions of IL-17s and the p53-family of proteins and are relevant to our understanding of neuroimmune mechanisms in cancer. They also reveal a DNA damage-independent function of CEP-1/p53 in invertebrate development and support the existence of a previously undescribed C. elegans dauer pathway.
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