Developmental plasticity and the response to nutrient stress in Caenorhabditis elegans

Rashid, Sabih; Wong, Christopher; Roy, Richard

doi:10.1016/j.ydbio.2021.01.015

Cited by 19 publications

(30 citation statements)

References 125 publications

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“…As a molecular hub for cellular metabolic control, AMPK is essential for controlling organism growth and development [ 22 , 39 , 49 ]. For instance, AMPK could promote protein phosphatase 2A (PP2A) during Bombyx mori and D. melanogaster metamorphosis in response to high amounts of 20-hydroxyecdysone (20E), resulting in limiting growth speed and body weight [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

“…In other words, AMPK maintains the balance of energy metabolism by regulating the synthesis and transformation of fat, protein, and glucose [ 18 , 19 , 20 , 21 ]. Furthermore, AMPK is in charge of maintaining germline quiescence in Caenorhabditis elegans larvae by changing the germline chromatin landscape to preserve germ cell integrity and regulating larvae metabolism to promote their smooth growth into adults [ 22 ]. When AMPK is activated, it enhances oxidative phosphorylation and the usage of pyruvate and allows Drosophila melanogaster to prune their dendrites of sensory neurons to complete developmental transitions [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

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AMPK Promotes Larval Metamorphosis of Mytilus coruscus

Zhang

Wang

et al. 2022

Genes

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Metamorphosis is a critical process in the transition from planktonic life to benthic life for marine invertebrates, which is accompanied by a large amount of energy consumption. Previous studies have proved that AMP-activated protein kinase (AMPK), as a vital energy regulator, plays a prominent role in mediating the growth and development of terrestrial animals. However, its function in the growth and development of marine invertebrates, especially in metamorphosis, remains elusive. This study explored the function of AMPK in the larval metamorphosis of Mytilus coruscus. The full-length cDNA of AMPK genes in M. coruscus was cloned and characterized, which is composed of three subunits, McAMPKα, McAMPKβ, and McAMPKγ. Pharmacological tests demonstrated that through the application of an AMPK activator, AMP substantially enhanced the larval metamorphosis rate (p < 0.05). By contrast, the larval metamorphosis rate decreased significantly after being treated with the AMPK inhibitor Compound C (p < 0.05). McAMPK gene knock-down resulted in a reduction in McAMPK gene expression (p < 0.05), and the larval metamorphosis of M. coruscus was significantly restrained (p < 0.05). These results indicated that AMPK signaling is vital in the larval metamorphosis of M. coruscus, which advances further understanding in exploring the molecular mechanisms in the metamorphosis of marine invertebrate larvae.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

AMPK Promotes Larval Metamorphosis of Mytilus coruscus

Zhang

Wang

et al. 2022

Genes

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“…C. elegans responds to starvation using multiple strategies during development [ 2 , 3 , 10 , 53 , 54 ]. Larvae respond to starvation by entering a developmental stage of arrest, known as dauer diapause, where animals reversibly arrest soma and germ line development, which resumes after refeeding [ 53 , 54 ]. Hermaphrodite L4 animals that encounter starvation can also slow germline development during the ‘germline starvation response’ (GSR) [ 2 , 3 , 10 ].…”

Section: Starvation and Germline Plasticitymentioning

confidence: 99%

Mechanisms of germ cell survival and plasticity in Caenorhabditis elegans

Cao

Pocock

2022

Biochemical Society Transactions

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Animals constantly encounter environmental and physiological stressors that threaten survival and fertility. Somatic stress responses and germ cell arrest/repair mechanisms are employed to withstand such challenges. The Caenorhabditis elegans germline combats stress by initiating mitotic germ cell quiescence to preserve genome integrity, and by removing meiotic germ cells to prevent inheritance of damaged DNA or to tolerate lack of germline nutrient supply. Here, we review examples of germline recovery from distinct stressors — acute starvation and defective splicing — where quiescent mitotic germ cells resume proliferation to repopulate a germ line following apoptotic removal of meiotic germ cells. These protective mechanisms reveal the plastic nature of germline stem cells.

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“…Moreover, proliferative activity of the C. elegans germline is highly sensitive to variation in physiology and the external environment, differing in response to nutrient quality and quantity, temperature, or social environment 17,30,[56][57][58][59][60] . Environmental variation modulates GSC proliferation via metabolic and sensory signaling pathways (e.g., TGF-β, TOR, AMPK and insulin), which act both dependently and independently of niche-mediated Delta/Notch signaling [61][62][63][64][65][66][67] . The C. elegans germ stem cell system is thus highly plastic, capable of fine-tuning its activity in response to subtle environmental changes.…”

Section: Introductionmentioning

confidence: 99%

Higher-order epistasis shapes natural variation in germ stem cell niche activity

Fausett

Sandjak

Billard

et al. 2022

Preprint

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Natural quantitative variation in developmental processes, such as cell proliferation, must be driven by allelic variation. Yet, the genotype-phenotype relationships underlying such trait variation are understudied due to their inherent complexity. Taking advantage of the simple Caenorhabditis elegans germline stem cell system, we used a quantitative genetic approach to characterize natural differences in germ stem cell niche activity of two distinct wild isolates, measured as differences in germline progenitor zone (PZ) size. Using quantitative trait locus (QTL) analysis, we detected multiple candidate loci, including two large-effect loci on chromosomes II and V. Resolving the chromosome V QTL, we discovered that the isolate with a smaller PZ exhibits a unique 148 base pair deletion in the promoter region of the Notch ligand, lag-2, a central signal promoting germ stem cell fate and proliferation. As predicted, introducing this deletion into the isolate with a large PZ resulted in significantly smaller PZ size. Unexpectedly, re-introducing the deleted ancestral sequence in the isolate with a smaller PZ caused PZ size to reduce even further. We show that these seemingly contradictory phenotypic effects are due to, partly antagonistic, epistatic interactions among the lag-2 promoter, the chromosome II QTL, and additional loci elsewhere in the genome. While we identified an obvious causal polymorphism explaining natural variation in germ stem cell niche activity, the effects of this variant became unpredictable due to higher-order epistasis. Studying the genetic architecture of quantitative developmental systems without taking into account its natural variation may be misleading, emphasizing the need for a better integration of developmental and quantitative genetics.

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Developmental plasticity and the response to nutrient stress in Caenorhabditis elegans

Cited by 19 publications

References 125 publications

AMPK Promotes Larval Metamorphosis of Mytilus coruscus

AMPK Promotes Larval Metamorphosis of Mytilus coruscus

Mechanisms of germ cell survival and plasticity in Caenorhabditis elegans

Higher-order epistasis shapes natural variation in germ stem cell niche activity

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