scholarly journals Hormonal Regulation of Diapause and Development in Nematodes, Insects, and Fishes

2021 ◽  
Vol 9 ◽  
Author(s):  
Xantha Karp
Keyword(s):  
Hormonal Regulation ◽  
Nuclear Hormone Receptor ◽  
Developmental Trajectory ◽  
Developmental Pathways ◽  
C Elegans ◽  
Developmental Arrest ◽  
Nothobranchius Furzeri ◽  
Animal Phyla ◽  
Diapause Development ◽  
Austrofundulus Limnaeus

Diapause is a state of developmental arrest adopted in response to or in anticipation of environmental conditions that are unfavorable for growth. In many cases, diapause is facultative, such that animals may undergo either a diapause or a non-diapause developmental trajectory, depending on environmental cues. Diapause is characterized by enhanced stress resistance, reduced metabolism, and increased longevity. The ability to postpone reproduction until suitable conditions are found is important to the survival of many animals, and both vertebrate and invertebrate species can undergo diapause. The decision to enter diapause occurs at the level of the whole animal, and thus hormonal signaling pathways are common regulators of the diapause decision. Unlike other types of developmental arrest, diapause is programmed, such that the diapause developmental trajectory includes a pre-diapause preparatory phase, diapause itself, recovery from diapause, and post-diapause development. Therefore, developmental pathways are profoundly affected by diapause. Here, I review two conserved hormonal pathways, insulin/IGF signaling (IIS) and nuclear hormone receptor signaling (NHR), and their role in regulating diapause across three animal phyla. Specifically, the species reviewed are Austrofundulus limnaeus and Nothobranchius furzeri annual killifishes, Caenorhabditis elegans nematodes, and insect species including Drosophila melanogaster, Culex pipiens, and Bombyx mori. In addition, the developmental changes that occur as a result of diapause are discussed, with a focus on how IIS and NHR pathways interact with core developmental pathways in C. elegans larvae that undergo diapause.

scholarly journals Environmental pheromone and endocrine signals correct heterochronic developmental phenotypes caused by insufficient expression of let-7 family microRNAs in C. elegans

2019 ◽  
Author(s):  
Orkan Ilbay ◽  
Victor Ambros
Keyword(s):  
Signaling Pathways ◽  
Cell Fate ◽  
Developmental Trajectories ◽  
Cell Lineage ◽  
Nuclear Hormone Receptor ◽  
Developmental Trajectory ◽  
Cell Fates ◽  
C Elegans ◽  
Developmental Progression ◽  
Endocrine Signaling

SummaryAdverse environmental conditions can affect rates of animal developmental progression and lead to temporary developmental quiescence (diapause), exemplified by the dauer larva stage of the nematode Caenorhabditis elegans. Remarkably, patterns of cell division and temporal cell fate progression in C. elegans larvae are not affected by changes in developmental trajectory. However, the underlying physiological and gene regulatory mechanisms that ensure robust developmental patterning despite substantial plasticity in developmental progression are largely unknown. Here, we report that diapause-inducing environmental pheromone and endocrine signals correct heterochronic developmental cell lineage defects caused by insufficient expression of let-7 family microRNAs in C. elegans. Two conserved endocrine signaling pathways, DAF-7/TGF-β and DAF-2/Insulin, that confer on the larva diapause/non-diapause alternative developmental trajectories, interact with the nuclear hormone receptor, DAF-12, to initiate and regulate a rewiring of the genetic circuitry controlling temporal cell fates. This rewiring includes: 1) repression of the DAF-12 ligand-activated expression of let-7 family microRNAs, and 2) engagement of a novel ligand-independent DAF-12 activity to downregulate the critical let-7 family target Hunchback-like-1 (HBL-1). This alternative HBL-1 downregulation program is responsible for correcting let-7 family insufficiency phenotypes and it requires the activities of certain heterochronic genes, lin-46, lin-4 and nhl-2, that are previously associated with an altered genetic program in post-diapause animals. Our results show how environmental pheromones and endocrine signaling pathways can coordinately regulate both developmental progression and cell fate transitions in C. elegans larvae under stress, so that the developmental schedule of cell fates remains unaffected by changes in developmental trajectory.

scholarly journals Rescue of a developmental arrest caused by a C. elegans heat-shock transcription-factor mutation by loss of ribosomal S6-kinase activity

2018 ◽  
Author(s):  
Peter Chisnell ◽  
T. Richard Parenteau ◽  
Elizabeth Tank ◽  
Kaveh Ashrafi ◽  
Cynthia Kenyon
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Heat Shock ◽  
Heat Shock Transcription Factor ◽  
Adult Longevity ◽  
Loss Of Function ◽  
S6 Kinase ◽  
Heat Shock Transcription Factors ◽  
C Elegans ◽  
Developmental Arrest

AbstractThe widely conserved heat-shock response, regulated by heat shock transcription factors, is not only essential for cellular stress resistance and adult longevity, but also for proper development. However, the genetic mechanisms by which heat-shock transcription factors regulate development are not well understood. In C. elegans, we conducted an unbiased genetic screen to identify mutations that could ameliorate the developmental arrest phenotype of a heat-shock factor mutant. Here we show that loss of the conserved translational activator rsks-1/S6-Kinase, a downstream effector of TOR kinase, can rescue the developmental-arrest phenotype of hsf-1 partial loss-of-function mutants. Unexpectedly, we show that the rescue is not likely caused by reduced translation, nor to activation of any of a variety of stress-protective genes and pathways. Our findings identify an as-yet unexplained regulatory relationship between the heat-shock transcription factor and the TOR pathway during C. elegans’ development.

scholarly journals Developmental pathways from child maltreatment to adolescent suicide-related behaviors: The internalizing and externalizing comorbidity hypothesis

2019 ◽  
Vol 32 (3) ◽  
pp. 945-959 ◽  
Author(s):  
Erinn Bernstein Duprey ◽  
Assaf Oshri ◽  
Sihong Liu
Keyword(s):  
Suicidal Ideation ◽  
Child Maltreatment ◽  
Childhood Abuse ◽  
Internalizing Symptoms ◽  
Developmental Trajectory ◽  
Developmental Pathways ◽  
Childhood And Adolescence ◽  
Adolescent Risk ◽  
And Behaviors ◽  
Internalizing And Externalizing

AbstractChild maltreatment is a robust risk factor for suicidal ideation and behaviors during adolescence. Elevations in internalizing and externalizing symptomology have been identified as two distinct developmental pathways linking child maltreatment and adolescent risk for suicide. However, recent research suggests that the co-occurrence of internalizing and externalizing symptomology may form a distinct etiological pathway for adolescent risk behaviors. Using the Longitudinal Studies on Child Abuse and Neglect (LONGSCAN) sample (N = 1,314), the present study employed a person-centered approach to identify patterns of concurrent change in internalizing and externalizing psychopathology over five time points from early childhood to adolescence in relation to previous experiences of child maltreatment and subsequent suicidal ideation and behaviors. Results indicated four distinct bivariate externalizing and internalizing growth trajectories. Group membership in a heightened comorbid internalizing and externalizing symptom trajectory mediated the association between childhood abuse and adolescent suicidal ideation and suicidal behaviors. These findings suggest that the concurrent development of externalizing and internalizing symptoms in childhood and adolescence may constitute a unique developmental trajectory that confers risk for suicide-related outcomes.

Hormonal components of altered developmental pathways in the annual killifish, Austrofundulus limnaeus

2011 ◽  
Vol 174 (2) ◽  
pp. 166-174 ◽  
Author(s):  
Benjamin M. Pri-Tal ◽  
Steven Blue ◽  
Francis K.-Y. Pau ◽  
Jason E. Podrabsky
Keyword(s):  
Developmental Pathways ◽  
Annual Killifish ◽  
Austrofundulus Limnaeus

scholarly journals Nuclear Hormone Receptor Regulation of MicroRNAs Controls Innate Immune Responses in C. elegans

2013 ◽  
Vol 9 (8) ◽  
pp. e1003545 ◽  
Author(s):  
Feng Liu ◽  
Chen-Xi He ◽  
Li-Jun Luo ◽  
Quan-Li Zou ◽  
Yong-Xu Zhao ◽  
...  
Keyword(s):  
Immune Responses ◽  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
Innate Immune ◽  
Receptor Regulation ◽  
Innate Immune Responses ◽  
C Elegans

scholarly journals Nuclear Hormone Receptor NHR-49 Controls Fat Consumption and Fatty Acid Composition in C. elegans

PLoS Biology ◽  
2005 ◽  
Vol 3 (2) ◽  
pp. e53 ◽  
Author(s):  
Marc R. Van Gilst ◽  
Haralambos Hadjivassiliou ◽  
Amber Jolly ◽  
Keith R Yamamoto
Keyword(s):  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Acid Composition ◽  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
C Elegans ◽  
Fat Consumption

scholarly journals Nuclear hormone receptor DHR96 mediates the resistance to xenobiotics but not the increased lifespan of insulin-mutant Drosophila

2016 ◽  
Vol 113 (5) ◽  
pp. 1321-1326 ◽  
Author(s):  
Sonita Afschar ◽  
Janne M. Toivonen ◽  
Julia Marianne Hoffmann ◽  
Luke Stephen Tain ◽  
Daniela Wieser ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Fruit Fly ◽  
Xenobiotic Metabolism ◽  
Nuclear Hormone Receptor ◽  
Laboratory Animals ◽  
Dietary Interventions ◽  
Gene Encoding ◽  
Transgenic Expression ◽  
C Elegans ◽  
Lipophilic Toxins

Lifespan of laboratory animals can be increased by genetic, pharmacological, and dietary interventions. Increased expression of genes involved in xenobiotic metabolism, together with resistance to xenobiotics, are frequent correlates of lifespan extension in the nematode worm Caenorhabditis elegans, the fruit fly Drosophila, and mice. The Green Theory of Aging suggests that this association is causal, with the ability of cells to rid themselves of lipophilic toxins limiting normal lifespan. To test this idea, we experimentally increased resistance of Drosophila to the xenobiotic dichlordiphenyltrichlorethan (DDT), by artificial selection or by transgenic expression of a gene encoding a cytochrome P450. Although both interventions increased DDT resistance, neither increased lifespan. Furthermore, dietary restriction increased lifespan without increasing xenobiotic resistance, confirming that the two traits can be uncoupled. Reduced activity of the insulin/Igf signaling (IIS) pathway increases resistance to xenobiotics and extends lifespan in Drosophila, and can also increase longevity in C. elegans, mice, and possibly humans. We identified a nuclear hormone receptor, DHR96, as an essential mediator of the increased xenobiotic resistance of IIS mutant flies. However, the IIS mutants remained long-lived in the absence of DHR96 and the xenobiotic resistance that it conferred. Thus, in Drosophila IIS mutants, increased xenobiotic resistance and enhanced longevity are not causally connected. The frequent co-occurrence of the two traits may instead have evolved because, in nature, lowered IIS can signal the presence of pathogens. It will be important to determine whether enhanced xenobiotic metabolism is also a correlated, rather than a causal, trait in long-lived mice.

Diapause in parasitic nematodes: a review

2002 ◽  
Vol 80 (11) ◽  
pp. 1817-1840 ◽  
Author(s):  
R I Sommerville ◽  
K G Davey
Keyword(s):  
Parasite Burden ◽  
Parasitic Nematodes ◽  
Second Phase ◽  
Fourth Stage ◽  
Environmental Signals ◽  
The Third ◽  
Developmental Arrest ◽  
Third Stage ◽  
Animal Hosts ◽  
Diapause Development

This review considers in a selective way the literature on diapause in parasitic nematodes, concentrating on four species of animal parasites and three species of plant parasites. We define diapause as a developmental arrest which is temporarily irreversible, so development will not resume, even under favourable conditions, until some intrinsic changes have been completed. Our analysis recognises four stages in diapause. The first is induction, typically brought about by environmental signals (although diapause may be genetically programmed independently of the environment). These environmental signals typically do not have an immediate effect on development, but we recognise a second phase, which we call the diapause pathway, in which worms have been induced to enter diapause at a later developmental stage. Surprisingly, entry into the diapause pathway may under some circumstances be reversible. The third stage is diapause development, a period during which development is suspended, but some ill-understood process must be completed prior to the fourth stage, emergence from diapause. Although diapause development is complete, resumption of development may be further delayed because of conditions in the host or in the environment: the worm is once more capable of development, but development is prevented by unfavourable conditions extrinsic to the worm. These may include the immune state of the host or the total parasite burden in animal hosts.

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