scholarly journals Genetic interactions between the DBL-1/BMP-like pathway and dpy body size–associated genes in Caenorhabditis elegans

2019 ◽  
Vol 30 (26) ◽  
pp. 3151-3160 ◽  
Author(s):  
Mohammed Farhan Lakdawala ◽  
Bhoomi Madhu ◽  
Lionel Faure ◽  
Mehul Vora ◽  
Richard W. Padgett ◽  
...  
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Bmp Signaling ◽  
Genetic Interactions ◽  
Set Domain ◽  
Downstream Targets ◽  
Ecm Proteins ◽  
Domain Protein

How BMP signaling and other body size regulators interact is not clear. We found interactions between Caenorhabditis elegans DBL-1/BMP and ECM, proteins that may modify or secrete DBL-1, and the SET domain protein BLMP-1. DBL-1 signaling may control downstream targets, some through BLMP-1, that affect size either directly or by feeding back on DBL-1 signaling.

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 Caenorhabditis elegans BMP Transcriptional Program Implicates Collagen Genes in Body Size Regulation

2017 ◽  
Author(s):  
Uday Madaan ◽  
Edlira Yzeiraj ◽  
Michael Meade ◽  
Christine A. Rushlow ◽  
Cathy Savage-Dunn
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Signaling Pathway ◽  
Transcriptional Network ◽  
Bmp Signaling ◽  
Functional Impairments ◽  
Size Regulation ◽  
Downstream Effectors ◽  
Bmp Pathway ◽  
Collagen Genes

AbstractBody size is a tightly regulated phenotype in metazoans that is dependent on both intrinsic and extrinsic factors. While signaling pathways such as insulin, Hippo, and myostatin are known to control organ and body size, the downstream effectors that mediate their effects are still poorly understood. In the nematode C. elegans, a Bone Morphogenetic Protein (BMP)-related signaling pathway is the major regulator of growth and body size. DBL-1, the BMP-related ligand, is secreted by neurons and body wall muscle, and acts as a dose-dependent regulator of body size. We investigated the transcriptional network through which the DBL-1/BMP pathway regulates body size and identified cuticle collagen genes as major effectors of growth control. Here we demonstrate that cuticle collagen genes can act as positive regulators (col-41), dose-sensitive regulators (rol-6), and negative regulators (col-141, col-142) of body size. Moreover, we show requirement of DBL-1/BMP signaling for stage-specific expression of cuticle collagen genes. We used chromatin immunoprecipitation followed by high throughput sequencing (ChIP-Seq) and electrophoretic mobility shift assays to show that the Smad signal transducers directly associate with conserved Smad binding elements in regulatory regions of col-141 and col-142, but not of col-41. Hence, cuticle collagen genes are directly and indirectly regulated via the DBL-1/BMP pathway. These results provide the first direct regulatory link between this conserved signaling pathway and the collagen genes that act as its downstream effectors in body size regulation. Since collagen mutations and misregulation are implicated in numerous human genetic disorders and injury sequelae, understanding how collagen gene expression is regulated has broad implications.Author SummaryBody size in humans and other animals is determined by the combined influence of genetic and environmental factors. Failure to regulate growth and body size appropriately can lead to a variety of functional impairments and reduced fitness. Progress has been made in identifying genetic determinants of body size, but these have not often been connected into functional pathways. In the nematode model Caenorhabditis elegans, single gene mutations in the BMP signaling pathway have profound effects on body size. Here we have elucidated the BMP transcriptional network and identified cuticle collagen genes as downstream effectors of body size regulation through the BMP pathway. Collagens play diverse roles in biology; mutations are often associated with rare heritable diseases such as osteogenesis imperfecta and Ehlers-Danlos syndrome. Our work thus connects a conserved signaling pathway with its critical downstream effectors, advancing insight into how body size is specified.

A BMP homolog acts as a dose-dependent regulator of body size and male tail patterning in Caenorhabditis elegans

Development ◽  
1999 ◽  
Vol 126 (2) ◽  
pp. 241-250 ◽  
Author(s):  
Y. Suzuki ◽  
M.D. Yandell ◽  
P.J. Roy ◽  
S. Krishna ◽  
C. Savage-Dunn ◽  
...  
Keyword(s):  
Body Size ◽  
Caenorhabditis Elegans ◽  
Expression Pattern ◽  
Genetic Interactions ◽  
Loss Of Function ◽  
Male Tail ◽  
C Elegans ◽  
Reduced Body ◽  
Smad Signaling Pathway ◽  
Dose Dependent

We cloned the dbl-1 gene, a C. elegans homolog of Drosophila decapentaplegic and vertebrate BMP genes. Loss-of-function mutations in dbl-1 cause markedly reduced body size and defective male copulatory structures. Conversely, dbl-1 overexpression causes markedly increased body size and partly complementary male tail phenotypes, indicating that DBL-1 acts as a dose-dependent regulator of these processes. Evidence from genetic interactions indicates that these effects are mediated by a Smad signaling pathway, for which DBL-1 is a previously unidentified ligand. Our study of the dbl-1 expression pattern suggests a role for neuronal cells in global size regulation as well as male tail patterning.

Depletion of a Novel SET-Domain Protein Enhances the Sterility of mes-3 and mes-4 Mutants of Caenorhabditis elegans

Genetics ◽  
2001 ◽  
Vol 159 (3) ◽  
pp. 1019-1029
Author(s):  
Lei Xu ◽  
Susan Strome
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Maternal Effect ◽  
Late Stage ◽  
Genetic Background ◽  
Set Domain ◽  
Germline Development ◽  
Associated Proteins ◽  
Alternatively Spliced ◽  
Domain Protein

Abstract Four maternal-effect sterile genes, mes-2, mes-3, mes-4, and mes-6, are essential for germline development in Caenorhabditis elegans. Homozygous mes progeny from heterozygous mothers are themselves fertile but produce sterile progeny with underproliferated and degenerated germlines. All four mes genes encode chromatin-associated proteins, two of which resemble known regulators of gene expression. To identify additional components in the MES pathway, we used RNA-mediated interference (RNAi) to test candidate genes for enhancement of the Mes mutant phenotype. Enhancement in this assay was induction of sterility a generation earlier, in the otherwise fertile homozygous progeny of heterozygous mothers, which previous results had suggested represent a sensitized genetic background. We tested seven genes predicted to encode regulators of chromatin organization for RNAi-induced enhancement of mes-3 sterility and identified one enhancer, called set-2 after the SET domain encoded by the gene. Depletion of SET-2 also enhances the sterile phenotype of mes-4 but not of mes-2 or mes-6. set-2 encodes two alternatively spliced transcripts, set-2l and set-2s, both of which are enriched in the germline of adults. In the adult germline, SET-2L protein is localized in mitotic and mid-late-stage meiotic nuclei but is undetectable in early pachytene nuclei. SET-2L protein is localized in all nuclei of embryos. The localization of SET-2L does not depend on any of the four MES proteins, and none of the MES proteins depend on SET-2 for their normal localization. Our results suggest that SET-2 participates along with the MES proteins in promoting normal germline development.

Interacting genes required for pharyngeal excitation by motor neuron MC in Caenorhabditis elegans.

Genetics ◽  
1995 ◽  
Vol 141 (4) ◽  
pp. 1365-1382 ◽  
Author(s):  
D M Raizen ◽  
R Y Lee ◽  
L Avery
Keyword(s):  
Caenorhabditis Elegans ◽  
Genetic Interactions ◽  
Neuron Type ◽  
Loss Of Function ◽  
Ach Release ◽  
Pharyngeal Muscle ◽  
Recessive Mutations ◽  
Allele Specific ◽  
Pharyngeal Pumping ◽  
Pumping Rates

Abstract We studied the control of pharyngeal excitation in Caenorhabditis elegans. By laser ablating subsets of the pharyngeal nervous system, we found that the MC neuron type is necessary and probably sufficient for rapid pharyngeal pumping. Electropharyngeograms showed that MC transmits excitatory postsynaptic potentials, suggesting that MC acts as a neurogenic pacemaker for pharyngeal pumping. Mutations in genes required for acetylcholine (ACh) release and an antagonist of the nicotinic ACh receptor (nAChR) reduced pumping rates, suggesting that a nAChR is required for MC transmission. To identify genes required for MC neurotransmission, we screened for mutations that cause slow pumping but no other defects. Mutations in two genes, eat-2 and eat-18, eliminated MC neurotransmission. A gain-of-function eat-18 mutation, ad820sd, and a putative loss-of-function eat-18 mutation, ad1110, both reduced the excitation of pharyngeal muscle in response to the nAChR agonists nicotine and carbachol, suggesting that eat-18 is required for the function of a pharyngeal nAChR. Fourteen recessive mutations in eat-2 fell into five complementation classes. We found allele-specific genetic interactions between eat-2 and eat-18 that correlated with complementation classes of eat-2. We propose that eat-18 and eat-2 function in a multisubunit protein complex involved in the function of a pharyngeal nAChR.

Caenorhabditis elegans auxilin: a J-domain protein essential for clathrin-mediated endocytosis in vivo

2001 ◽  
Vol 3 (2) ◽  
pp. 215-219 ◽  
Author(s):  
Tsvika Greener ◽  
Barth Grant ◽  
Yinhua Zhang ◽  
Xufeng Wu ◽  
Lois E. Greene ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
J Domain ◽  
Domain Protein
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