scholarly journals Rictor/TORC2 Regulates Caenorhabditis elegans Fat Storage, Body Size, and Development through sgk-1

PLoS Biology ◽  
2009 ◽  
Vol 7 (3) ◽  
pp. e1000060 ◽  
Author(s):  
Kevin T Jones ◽  
Elisabeth R Greer ◽  
David Pearce ◽  
Kaveh Ashrafi
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Fat Storage ◽  
Storage Body

scholarly journals Regulation of Fat Storage and Reproduction by Krüppel-Like Transcription Factor KLF3 and Fat-Associated Genes in Caenorhabditis elegans

2011 ◽  
Vol 411 (3) ◽  
pp. 537-553 ◽  
Author(s):  
Jun Zhang ◽  
Razan Bakheet ◽  
Ranjit S. Parhar ◽  
Cheng-Han Huang ◽  
M. Mahmood Hussain ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Caenorhabditis Elegans ◽  
Fat Storage

The control of cell growth and body size in Caenorhabditis elegans

2014 ◽  
Vol 321 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Simon Tuck
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Cell Growth

scholarly journals A conserved family of proteins facilitates nascent lipid droplet budding from the ER

2015 ◽  
Vol 211 (2) ◽  
pp. 261-271 ◽  
Author(s):  
Vineet Choudhary ◽  
Namrata Ojha ◽  
Andy Golden ◽  
William A. Prinz
Keyword(s):  
Electron Microscopy ◽  
Endoplasmic Reticulum ◽  
Lipid Metabolism ◽  
Caenorhabditis Elegans ◽  
Lipid Droplet ◽  
Lipid Droplets ◽  
De Novo ◽  
Fat Storage ◽  
Higher Eukaryotes ◽  
Er Membrane

Lipid droplets (LDs) are found in all cells and play critical roles in lipid metabolism. De novo LD biogenesis occurs in the endoplasmic reticulum (ER) but is not well understood. We imaged early stages of LD biogenesis using electron microscopy and found that nascent LDs form lens-like structures that are in the ER membrane, raising the question of how these nascent LDs bud from the ER as they grow. We found that a conserved family of proteins, fat storage-inducing transmembrane (FIT) proteins, is required for proper budding of LDs from the ER. Elimination or reduction of FIT proteins in yeast and higher eukaryotes causes LDs to remain in the ER membrane. Deletion of the single FIT protein in Caenorhabditis elegans is lethal, suggesting that LD budding is an essential process in this organism. Our findings indicated that FIT proteins are necessary to promote budding of nascent LDs from the ER.

scholarly journals lon-1 Regulates Caenorhabditis elegans Body Size Downstream of the dbl-1 TGFβ Signaling Pathway

2002 ◽  
Vol 246 (2) ◽  
pp. 418-428 ◽  
Author(s):  
Lisa L. Maduzia ◽  
Tina L. Gumienny ◽  
Cole M. Zimmerman ◽  
Huang Wang ◽  
Pradnya Shetgiri ◽  
...  
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Signaling Pathway ◽  
Tgfβ Signaling ◽  
Tgfβ Signaling Pathway

scholarly journals Non-stringent tissue-source requirements for BMP ligand expression in regulation of body size in Caenorhabditis elegans

2011 ◽  
Vol 93 (6) ◽  
pp. 427-432 ◽  
Author(s):  
CATHY SAVAGE-DUNN ◽  
LING YU ◽  
KWESI GILL ◽  
MUHAMMAD AWAN ◽  
THILINI FERNANDO
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Small Body ◽  
Ectopic Expression ◽  
Target Tissue ◽  
Signal Transducers ◽  
Endogenous Expression ◽  
Adult Growth ◽  
Morphogenetic Protein ◽  
Ligand Expression

SummaryIn Caenorhabditis elegans, the Bone Morphogenetic Protein (BMP)-related ligand Dpp- and BMP-like-1 (DBL-1) regulates body size by promoting the larval and adult growth of the large epidermal syncytium hyp7 without affecting cell division. This system provides an excellent model for dissecting the growth-promoting activities of BMP ligands, since in this context the growth and differentiation functions of DBL-1 are naturally uncoupled. dbl-1 is expressed primarily in neurons and the DBL-1 ligand signals to its receptors and Smad signal transducers in the target tissue of the epidermis. The requirements constraining the source(s) of DBL-1, however, have not previously been investigated. We show here that dbl-1 expression requirements are strikingly relaxed. Expression in non-overlapping subsets of the endogenous expression pattern, as well as ectopic expression, can provide sufficient levels of activity for rescue of the small body size of dbl-1 mutants. By analysing dbl-1 expression levels in transgenic strains with different degrees of rescue, we corroborate the model that DBL-1 is a dose-dependent regulator of growth. We conclude that, for body size regulation, the site of expression of dbl-1 is less important than the level of expression.

scholarly journals Cell size and fat content of dietary-restricted Caenorhabditis elegans are regulated by ATX-2, an mTOR repressor

2016 ◽  
Vol 113 (32) ◽  
pp. E4620-E4629 ◽  
Author(s):  
Daniel Z. Bar ◽  
Chayki Charar ◽  
Jehudith Dorfman ◽  
Tam Yadid ◽  
Lionel Tafforeau ◽  
...  
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Cell Size ◽  
Fat Content ◽  
Mtor Pathway ◽  
The Body ◽  
Dependent Growth ◽  
Multiple Species ◽  
Amp Activated Protein Kinase ◽  
Gdp Dissociation Inhibitor

Dietary restriction (DR) is a metabolic intervention that extends the lifespan of multiple species, including yeast, flies, nematodes, rodents, and, arguably, rhesus monkeys and humans. Hallmarks of lifelong DR are reductions in body size, fecundity, and fat accumulation, as well as slower development. We have identified atx-2, the Caenorhabditis elegans homolog of the human ATXN2L and ATXN2 genes, as the regulator of these multiple DR phenotypes. Down-regulation of atx-2 increases the body size, cell size, and fat content of dietary-restricted animals and speeds animal development, whereas overexpression of atx-2 is sufficient to reduce the body size and brood size of wild-type animals. atx-2 regulates the mechanistic target of rapamycin (mTOR) pathway, downstream of AMP-activated protein kinase (AMPK) and upstream of ribosomal protein S6 kinase and mTOR complex 1 (TORC1), by its direct association with Rab GDP dissociation inhibitor β, which likely regulates RHEB shuttling between GDP-bound and GTP-bound forms. Taken together, this work identifies a previously unknown mechanism regulating multiple aspects of DR, as well as unknown regulators of the mTOR pathway. They also extend our understanding of diet-dependent growth retardation, and offers a potential mechanism to treat obesity.

scholarly journals crm-1 facilitates BMP signaling to control body size in Caenorhabditis elegans

2007 ◽  
Vol 311 (1) ◽  
pp. 95-105 ◽  
Author(s):  
Wong Yan Fung ◽  
Ko Frankie Chi Fat ◽  
Cheah Kathryn Song Eng ◽  
Chow King Lau
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Bmp Signaling ◽  
Control Body

scholarly journals Dopamine regulates body size in Caenorhabditis elegans

2016 ◽  
Vol 412 (1) ◽  
pp. 128-138 ◽  
Author(s):  
Takashi Nagashima ◽  
Eitaro Oami ◽  
Natsumaro Kutsuna ◽  
Shoichi Ishiura ◽  
Satoshi Suo
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans

scholarly journals Lamin regulates the dietary restriction response via the mTOR pathway in Caenorhabditis elegans

2021 ◽  
Author(s):  
Chayki Charar ◽  
Sally Metsuyanim-Cohen ◽  
Daniel Z. Bar
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Life Span ◽  
Dietary Restriction ◽  
Metabolic Regulation ◽  
Fat Content ◽  
Mtor Pathway ◽  
Reduced Body ◽  
Animal Size ◽  
Mtor Complex 1

Animals subjected to dietary restriction (DR) have reduced body size, low fecundity, slower development, lower fat content and longer life span. We identified lamin as a regulator of multiple dietary restriction phenotypes. Downregulation of lmn-1, the single Caenorhabditis elegans lamin gene, increased animal size and fat content, specifically in DR animals. The LMN-1 protein acts in the mTOR pathway, upstream to RAPTOR and S6K, key component and target of mTOR complex 1 (mTORC1), respectively. DR excludes the mTORC1 activator RAGC-1 from the nucleus. Downregulation of lmn-1 restores RAGC-1 to the nucleus, a necessary step for the activation of the mTOR pathway. These findings further link lamin to metabolic regulation.

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