The Caenorhabditis elegans NK-2 homeobox gene ceh-22 activates pharyngeal muscle gene expression in combination with pha-1 and is required for normal pharyngeal development

Development ◽  
1997 ◽  
Vol 124 (20) ◽  
pp. 3965-3973 ◽  
Author(s):  
P.G. Okkema ◽  
E. Ha ◽  
C. Haun ◽  
W. Chen ◽  
A. Fire
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Muscle Development ◽  
Synergistic Effects ◽  
Chain Gene ◽  
Loss Of Function ◽  
Pharyngeal Muscle ◽  
Muscle Gene Expression ◽  
Pharyngeal Muscles ◽  
Muscle Gene

Pharyngeal muscle development in the nematode Caenorhabditis elegans appears to share similarities with cardiac muscle development in other species. We have previously described CEH-22, an NK-2 class homeodomain transcription factor similar to Drosophila tinman and vertebrate Nkx2-5, which is expressed exclusively in the pharyngeal muscles. In vitro, CEH-22 binds the enhancer from myo-2, a pharyngeal muscle-specific myosin heavy chain gene. In this paper, we examine the role CEH-22 plays in pharyngeal muscle development and gene activation by (a) ectopically expressing ceh-22 in transgenic C. elegans and (b) examining the phenotype of a ceh-22 loss-of-function mutant. These experiments indicate that CEH-22 is an activator of myo-2 expression and that it is required for normal pharyngeal muscle development. However, ceh-22 is necessary for neither formation of the pharyngeal muscles, nor for myo-2 expression. Our data suggest parallel and potentially compensating pathways contribute to pharyngeal muscle differentiation. We also examine the relationship between ceh-22 and the pharyngeal organ-specific differentiation gene pha-1. Mutations in ceh-22 and pha-1 have strongly synergistic effects on pharyngeal muscle gene expression; in addition, a pha-1 mutation enhances the lethal phenotype caused by a mutation in ceh-22. Wild-type pha-1 is not required for the onset of ceh-22 expression but it appears necessary for maintained expression of ceh-22.

scholarly journals The Caenorhabditis elegans NK-2 class homeoprotein CEH-22 is involved in combinatorial activation of gene expression in pharyngeal muscle

Development ◽  
1994 ◽  
Vol 120 (8) ◽  
pp. 2175-2186 ◽  
Author(s):  
P.G. Okkema ◽  
A. Fire
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Specific Activity ◽  
Myogenic Differentiation ◽  
Smooth Muscles ◽  
Chain Gene ◽  
Cdna Expression Library ◽  
Homeodomain Protein ◽  
Pharyngeal Muscle ◽  
Pharyngeal Muscles

The pharyngeal muscles of Caenorhabditis elegans are single sarcomere muscles used for feeding. Like vertebrate cardiac and smooth muscles, C. elegans pharyngeal muscle does not express any of the known members of the MyoD family of myogenic factors. To identify mechanisms regulating gene expression in this tissue, we have characterized a pharyngeal muscle-specific enhancer from myo-2, a myosin heavy chain gene expressed exclusively in pharyngeal muscle. Assaying enhancer function in transgenic animals, we identified three subelements, designated A, B and C, that contribute to myo-2 enhancer activity. These subelements are individually inactive; however, any combination of two or more subelements forms a functional enhancer. The B and C subelements have distinct cell type specificities. A duplication of B activates transcription in a subset of pharyngeal muscles (m3, m4, m5 and m7). A duplication of C activates transcription in all pharyngeal cells, muscle and non-muscle. Thus, the activity of the myo-2 enhancer is regulated by a combination of pharyngeal muscle-type-specific and organ-specific signals. Screening a cDNA expression library, we identified a gene encoding an NK-2 class homeodomain protein, CEH-22, that specifically binds a site necessary for activity of the B subelement. CEH-22 protein is first expressed prior to myogenic differentiation and is present in the same subset of pharyngeal muscles in which B is active. Expression continues throughout embryonic and larval development. This expression pattern suggests CEH-22 plays a key role in pharyngeal muscle-specific activity of the myo-2 enhancer.

scholarly journals Age and Sex-Dependent ADNP Regulation of Muscle Gene Expression Is Correlated with Motor Behavior: Possible Feedback Mechanism with PACAP

2020 ◽  
Vol 21 (18) ◽  
pp. 6715 ◽  
Author(s):  
Oxana Kapitansky ◽  
Shlomo Sragovich ◽  
Iman Jaljuli ◽  
Adva Hadar ◽  
Eliezer Giladi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Muscle Development ◽  
Motor Behavior ◽  
Expression Patterns ◽  
Feedback Mechanism ◽  
Bladder Function ◽  
Drug Candidate ◽  
Specific Gene ◽  
Muscle Gene Expression ◽  
Muscle Gene

The activity-dependent neuroprotective protein (ADNP), a double-edged sword, sex-dependently regulates multiple genes and was previously associated with the control of early muscle development and aging. Here we aimed to decipher the involvement of ADNP in versatile muscle gene expression patterns in correlation with motor function throughout life. Using quantitative RT-PCR we showed that Adnp+/− heterozygous deficiency in mice resulted in aberrant gastrocnemius (GC) muscle, tongue and bladder gene expression, which was corrected by the Adnp snippet, drug candidate, NAP (CP201). A significant sexual dichotomy was discovered, coupled to muscle and age-specific gene regulation. As such, Adnp was shown to regulate myosin light chain (Myl) in the gastrocnemius (GC) muscle, the language acquisition gene forkhead box protein P2 (Foxp2) in the tongue and the pituitary-adenylate cyclase activating polypeptide (PACAP) receptor PAC1 mRNA (Adcyap1r1) in the bladder, with PACAP linked to bladder function. A tight age regulation was observed, coupled to an extensive correlation to muscle function (gait analysis), placing ADNP as a muscle-regulating gene/protein.

scholarly journals Skeletal muscle gene expression after myostatin knockout in mature mice

2009 ◽  
Vol 38 (3) ◽  
pp. 342-350 ◽  
Author(s):  
Stephen Welle ◽  
Andrew Cardillo ◽  
Michelle Zanche ◽  
Rabi Tawil
Keyword(s):  
Gene Expression ◽  
Muscle Development ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Muscle Gene Expression ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Muscle Gene ◽  
Or Genes ◽  
And Control

There is much interest in developing anti-myostatin agents to reverse or prevent muscle atrophy in adults, so it is important to characterize the effects of reducing myostatin activity after normal muscle development. For assessment of the effect of loss of myostatin signaling on gene expression in muscle, RNA from mice with postdevelopmental myostatin knockout was analyzed with oligonucleotide microarrays. Myostatin was undetectable in muscle within 2 wk after Cre recombinase activation in 4-month-old male mice with floxed myostatin genes. Three months after myostatin depletion, muscle mass had increased 26% (vs. 2% after induction of Cre activity in mice with normal myostatin genes), at which time the expression of several hundred genes differed in knockout and control mice at nominal P < 0.01. In contrast to previously reported effects of constitutive myostatin knockout, postdevelopmental knockout did not downregulate expression of genes encoding slow isoforms of contractile proteins or genes encoding proteins involved in energy metabolism. Several collagen genes were expressed at 20–50% lower levels in the myostatin-deficient muscles, which had ∼25% less collagen than normal muscles as reflected by hydroxyproline content. Most of the other genes affected by myostatin depletion have not been previously linked to myostatin signaling. Gene set enrichment analysis suggested that Smads are not the only transcription factors with reduced activity after myostatin depletion. These data reinforce other evidence that myostatin regulates collagen production in muscle and demonstrate that many of the previously reported effects of constitutive myostatin deficiency do not occur when myostatin is knocked out in mature muscles.

scholarly journals The Caenorhabditis elegans paxillin orthologue, PXL-1, is required for pharyngeal muscle contraction and for viability

2011 ◽  
Vol 22 (14) ◽  
pp. 2551-2563 ◽  
Author(s):  
Adam Warner ◽  
Hiroshi Qadota ◽  
Guy M. Benian ◽  
A. Wayne Vogl ◽  
Donald G. Moerman
Keyword(s):  
Caenorhabditis Elegans ◽  
Body Wall ◽  
Fluorescent Protein ◽  
Repeat Unit ◽  
Body Wall Muscle ◽  
Loss Of Function ◽  
Pharyngeal Muscle ◽  
Adhesion Sites ◽  
Pharyngeal Muscles ◽  
Green Fluorescent

We have identified the gene C28H8.6 (pxl-1) as the Caenorhabditis elegans orthologue of vertebrate paxillin. PXL-1 contains the four C-terminal LIM domains conserved in paxillin across all species and three of the five LD motifs found in the N-terminal half of most paxillins. In body wall muscle, PXL-1 antibodies and a full-length green fluorescent protein translational fusion localize to adhesion sites in the sarcomere, the functional repeat unit in muscle responsible for contraction. PXL-1 also localizes to ring-shaped structures near the sarcolemma in pharyngeal muscle corresponding to podosome-like sites of actin attachment. Our analysis of a loss-of-function allele of pxl-1, ok1483, shows that loss of paxillin leads to early larval arrested animals with paralyzed pharyngeal muscles and eventual lethality, presumably due to an inability to feed. We rescued the mutant phenotype by expressing paxillin solely in the pharynx and found that these animals survived and are essentially wild type in movement and body wall muscle structure. This indicates a differential requirement for paxillin in these two types of muscle. In pharyngeal muscle it is essential for contraction, whereas in body wall muscle it is dispensable for filament assembly, sarcomere stability, and ultimately movement.

scholarly journals Circulating leptin and its muscle gene expression in Nellore cattle with divergent feed efficiency

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Lúcio Flávio Macedo Mota ◽  
Cristina Moreira Bonafé ◽  
Pâmela Almeida Alexandre ◽  
Miguel Henrique Santana ◽  
Francisco José Novais ◽  
...  
Keyword(s):  
Gene Expression ◽  
Feed Efficiency ◽  
Muscle Gene Expression ◽  
Nellore Cattle ◽  
Muscle Gene

scholarly journals Kruppel-like Factor 4 Abrogates Myocardin-induced Activation of Smooth Muscle Gene Expression

2005 ◽  
Vol 280 (10) ◽  
pp. 9719-9727 ◽  
Author(s):  
Yan Liu ◽  
Sanjay Sinha ◽  
Oliver G. McDonald ◽  
Yueting Shang ◽  
Mark H. Hoofnagle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Muscle Gene Expression ◽  
Muscle Gene

Skeletal muscle gene expression in space‐flown rats

2004 ◽  
Vol 18 (3) ◽  
pp. 522-524 ◽  
Author(s):  
Takeshi Nikawa ◽  
Kazumi Ishidoh ◽  
Katsuya Hirasaka ◽  
Ibuki Ishihara ◽  
Madoka Ikemoto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Muscle Gene Expression ◽  
Muscle Gene
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