Disease relevance of Pharyngeal Muscles

• The high prevalence of seizure disorders, gastroesophageal reflux with the risk of aspiration, and airway complications related to poor pharyngeal muscle control are of concern to the anaesthetist [1].
• On the basis of clinical observations of patients treated perioperatively with dantrolene sodium for malignant hyperthermia, we hypothesized that pharyngeal muscle spasms are a major factor in tonsillectomy pain [2].
• Recent data suggest that mild degrees of residual paresis (train-of-four TOF ratios of 0.7-0.9) may be associated with significant impairment of respiratory and pharyngeal muscle function [3].

Psychiatry related information on Pharyngeal Muscles

• This is suggested to be essential defects for olfaction. gsc mutant mice also show several pharyngeal phenotypes, including defects in the pharyngeal muscles and the pharyngeal mucosa [4].

High impact information on Pharyngeal Muscles

• We have isolated and characterized the C. elegans gene eat-5, which is required for synchronized pharyngeal muscle contractions, and find that it is a new member of this family [5].
• Development of pharyngeal muscle in nematodes and cardiac muscle in vertebrates and insects involves the related homeobox genes ceh-22, nkx2.5, and tinman, respectively [6].
• Using a dyn-1::lacZ gene fusion, a high level of dynamin expression was observed in motor neurons, intestine, and pharyngeal muscle [7].
• We show that expression of the beta 3-tubulin gene in the somatic muscles, the pharyngeal muscles, and the dorsal vessel is mediated by far upstream sequences [8].
• MHC C and MHC D are exclusively produced in the pharyngeal muscle [9].

Biological context of Pharyngeal Muscles

• 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 [10].
• Because de209 enhancer activity is primarily limited to the pharyngeal muscles, we hypothesize that de209 also binds factors functioning with PHA-4 to specifically activate ceh-22 expression in pharyngeal muscle [11].
• Gene expression in the pharyngeal muscles of C. elegans is regulated in part by the NK-2 family homeodomain factor CEH-22, which is structurally and functionally related to Drosophila Tinman and the vertebrate Nkx2-5 factors. ceh-22 is expressed exclusively in the pharyngeal muscles and is the earliest gene known to be expressed in this tissue [12].

Anatomical context of Pharyngeal Muscles

• The unc-89 complex transcription unit contains at least three promoters: one directing UNC-89-A and -B primarily in body-wall and pharyngeal muscle, one internal promoter directing expression of UNC-89-C primarily in body-wall muscle, and one internal promoter directing expression of UNC-89-D primarily in a few muscle cells of the tail [13].
• In eat-5 mutants the motions of the different parts of the pharynx were poorly synchronized. eat-6 and eat-12 mutants failed to relax their pharyngeal muscles properly [14].
• C. elegans BIP was expressed in pharyngeal muscle, hypodermis and several neuronal cells, an expression pattern overlaps with those of BRA-1 and BRA-2 [15].
• To evaluate the influence of upper airway sensory feedback on pharyngeal muscle tone and thus pharyngeal patency, we measured pharyngeal airflow resistance and breathing pattern in 15 normal, supine subjects before and after topical lidocaine anesthesia of the pharynx and glottis [16].

Associations of Pharyngeal Muscles with chemical compounds

• EAT-2 is a nicotinic acetylcholine receptor subunit that functions in the pharyngeal muscle [17].
• Normal glucose uptake by tongue and pharyngeal muscles in FDG-PET imaging [18].
• High levels of signaling through GAR-3 inhibit pharyngeal muscle relaxation and impair feeding--but do not block muscle repolarization--when worms are exposed to arecoline, a muscarinic agonist [19].
• 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 [20].
• Serotonin regulates repolarization of the C. elegans pharyngeal muscle [21].

Gene context of Pharyngeal Muscles

• Functions of mlc-1 are redundant to those of mlc-2 in both body-wall and pharyngeal muscle. mlc-1(0) mutants are wild type, but mlc-1(0) mlc-2(0) double mutants arrest as incompletely elongated L1 larvae, having both pharyngeal and body-wall muscle defects [22].
• The src-1 and csk-1 genes are co-expressed in some head neurons, the anchor cell and the tail region, while kin-22 and csk-1 genes are co-expressed in pharyngeal muscles and tail region [23].
• However, ceh-22 is necessary for neither formation of the pharyngeal muscles, nor for myo-2 expression [10].
• 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 [10].
• We found that eff-1 is necessary to initiate and expand multiple microfusion events between pharyngeal muscle cells [24].

References