Development of Full Sweet, Umami, and Bitter Taste Responsiveness Requires Regulator of G protein Signaling-21 (RGS21)

Schroer, Adam B.; Gross, Joshua; Kaski, Shane W; Wix, Kim; Siderovski, David P.; Vandenbeuch, Aurélie; Setola, Vincent

doi:10.1093/chemse/bjy024

Cited by 8 publications

(4 citation statements)

References 71 publications

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“…Glucagon-like peptide-1, glucagon, neuropeptide Y, cholecystokinin, and vasoactive intestinal peptide were identified inside TBs. Each gut hormone and its cognate receptor were restricted to subpopulations of TBCs and associated nerve fibers [ 11 , 24 , 69 , 70 , 71 , 72 , 73 ].…”

Section: Discussionmentioning

confidence: 99%

Glucagon-Like Peptide 1 and Taste Perception: From Molecular Mechanisms to Potential Clinical Implications

Jensterle

Rizzo

2021

IJMS

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Preclinical studies provided some important insights into the action of glucagon-like peptide 1 (GLP-1) in taste perception. This review examines the literature to uncover some molecular mechanisms and connections between GLP-1 and the gustatory coding. Local GLP-1 production in the taste bud cells, the expression of GLP-1 receptor on the adjacent nerves, a functional continuum in the perception of sweet chemicals from the gut to the tongue and an identification of GLP-1 induced signaling pathways in peripheral and central gustatory coding all strongly suggest that GLP-1 is involved in the taste perception, especially sweet. However, the impact of GLP-1 based therapies on gustatory coding in humans remains largely unaddressed. Based on the molecular background we encourage further exploration of the tongue as a new treatment target for GLP-1 receptor agonists in clinical studies. Given that pharmacological manipulation of gustatory coding may represent a new potential strategy against obesity and diabetes, the topic is of utmost clinical relevance.

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Section: Discussionmentioning

confidence: 99%

Glucagon-Like Peptide 1 and Taste Perception: From Molecular Mechanisms to Potential Clinical Implications

Jensterle

Rizzo

2021

IJMS

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“…RNA extraction and qRT-PCR procedures were previously described by Schroer et al . [38]. Briefly, TRIzol reagent (Invitrogen) was used to extract RNA from both tissue and cells.…”

Section: Methodsmentioning

confidence: 99%

A role for Regulator of G protein Signaling-12 (RGS12) in the balance between myoblast proliferation and differentiation

et al. 2019

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Regulators of G Protein Signaling (RGS proteins) inhibit G protein-coupled receptor (GPCR) signaling by accelerating the GTP hydrolysis rate of activated Gα subunits. Some RGS proteins exert additional signal modulatory functions, and RGS12 is one such protein, with five additional, functional domains: a PDZ domain, a phosphotyrosine-binding domain, two Ras-binding domains, and a Gα·GDP-binding GoLoco motif. RGS12 expression is temporospatially regulated in developing mouse embryos, with notable expression in somites and developing skeletal muscle. We therefore examined whether RGS12 is involved in the skeletal muscle myogenic program. In the adult mouse, RGS12 is expressed in the tibialis anterior (TA) muscle, and its expression is increased early after cardiotoxin-induced injury, suggesting a role in muscle regeneration. Consistent with a potential role in coordinating myogenic signals, RGS12 is also expressed in primary myoblasts; as these cells undergo differentiation and fusion into myotubes, RGS12 protein abundance is reduced. Myoblasts isolated from mice lacking Rgs12 expression have an impaired ability to differentiate into myotubes ex vivo , suggesting that RGS12 may play a role as a modulator/switch for differentiation. We also assessed the muscle regenerative capacity of mice conditionally deficient in skeletal muscle Rgs12 expression (via Pax7 -driven Cre recombinase expression), following cardiotoxin-induced damage to the TA muscle. Eight days post-damage, mice lacking RGS12 in skeletal muscle had attenuated repair of muscle fibers. However, when mice lacking skeletal muscle expression of Rgs12 were cross-bred with mdx mice (a model of human Duchenne muscular dystrophy), no increase in muscle degeneration was observed over time. These data support the hypothesis that RGS12 plays a role in coordinating signals during the myogenic program in select circumstances, but loss of the protein may be compensated for within model syndromes of prolonged bouts of muscle damage and repair.

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“…RGS21 is also expressed in bitter taste receptor-expressing cells in the airway epithelium and was shown to tone down bitter taste receptor signaling in these cells [ 106 ]. Interestingly, global RGS21 deletion in mice caused reduced responses to bitter, sweet umami, and salty tastants [ 107 , 108 ]. This result is opposite of what is expected for a negative regulator and may reflect abnormalities in development and regeneration of the taste system or in expression of other taste signaling machinery components in the absence of this key signaling protein.…”

Section: Regulation Of Sweet Taste Signalingmentioning

confidence: 99%

Sweet Taste Signaling: The Core Pathways and Regulatory Mechanisms

Sukumaran

Palayyan

2022

IJMS

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Sweet taste, a proxy for sugar-derived calories, is an important driver of food intake, and animals have evolved robust molecular and cellular machinery for sweet taste signaling. The overconsumption of sugar-derived calories is a major driver of obesity and other metabolic diseases. A fine-grained appreciation of the dynamic regulation of sweet taste signaling mechanisms will be required for designing novel noncaloric sweeteners with better hedonic and metabolic profiles and improved consumer acceptance. Sweet taste receptor cells express at least two signaling pathways, one mediated by a heterodimeric G-protein coupled receptor encoded by taste 1 receptor members 2 and 3 (TAS1R2 + TAS1R3) genes and another by glucose transporters and the ATP-gated potassium (KATP) channel. Despite these important discoveries, we do not fully understand the mechanisms regulating sweet taste signaling. We will introduce the core components of the above sweet taste signaling pathways and the rationale for having multiple pathways for detecting sweet tastants. We will then highlight the roles of key regulators of the sweet taste signaling pathways, including downstream signal transduction pathway components expressed in sweet taste receptor cells and hormones and other signaling molecules such as leptin and endocannabinoids.

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Development of Full Sweet, Umami, and Bitter Taste Responsiveness Requires Regulator of G protein Signaling-21 (RGS21)

Cited by 8 publications

References 71 publications

Glucagon-Like Peptide 1 and Taste Perception: From Molecular Mechanisms to Potential Clinical Implications

Glucagon-Like Peptide 1 and Taste Perception: From Molecular Mechanisms to Potential Clinical Implications

A role for Regulator of G protein Signaling-12 (RGS12) in the balance between myoblast proliferation and differentiation

Sweet Taste Signaling: The Core Pathways and Regulatory Mechanisms

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