Inward rectifier channel, ROMK, is localized to the apical tips of glial‐like cells in mouse taste buds

Dvoryanchikov, Gennady; Sinclair, Michael S.; Perea-Martinez, Isabel; Wang, Tong; Chaudhari, Nirupa

doi:10.1002/cne.22196

Cited by 7 publications

(7 citation statements)

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“…Our results are consistent with previous reports from in vitro studies, and we are the first to demonstrate the functional difference between ROMK1 and ROMK2 in regulation of Na and K homeostasis in vivo. No specific role for the extended N terminus of ROMK3 has yet been identified, and we were not able to detect any ROMK3 expression in the kidneys of either WT, as reported previously (35), or Romk1 KO mice by Q-PCR.…”

Section: Discussionsupporting

confidence: 46%

Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion

Dong

Yan

et al. 2016

Journal of Biological Chemistry

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Romk knock-out mice show a similar phenotype to Bartter syndrome of salt wasting and dehydration due to reduced Na-K2Cl-cotransporter activity. At least three ROMK isoforms have been identified in the kidney; however, unique functions of any of the isoforms in nephron segments are still poorly understood. We have generated a mouse deficient only in Romk1 by selective deletion of the Romk1-specific first exon using an ES cell CreLoxP strategy and examined the renal phenotypes, ion transporter expression, ROMK channel activity, and localization under normal and high K intake. The renal outer medullary potassium channel (ROMK) 3 is an ATP-dependent potassium channel (Kir1.1) that forms apical K channels that play an important role in K ϩ recycling to support sodium and chloride absorption in the thick ascending limb (TAL), and in regulation of K ϩ secretion in the collecting duct (CD). Mutations in the ROMK channel cause Type II Bartter syndrome that presents with polyhydramnios and postnatal life threatening volume depletion caused by loss of salt reabsorbing capacity by the thick ascending limb (1). Romk knock-out mice, originally generated from Gary Shull's lab at the University of Cincinnati, exhibited the same phenotypes as the Bartter syndrome in humans (2). By using the Romk Bartter mouse model, we have further confirmed that ROMK forms both small conductance K ϩ channels (SK) and 70 pS K channels in apical membranes of the thick ascending limb and cortical collecting duct (3, 4). We have demonstrated: 1) absence of both SK activity and 70 pS K ϩ channels in apical membranes of thick ascending limb and cortical collecting duct in Romk knock-out mice; 2) Romk knock-out mice produced similar phenotypes to Bartter syndrome consisting of salt and water wasting due to reduced NKCC2 activity and expression (3, 5); 3) the salt and water wasting from the kidney is compensated by increased thiazide-sensitive NaCl transport expression and activity, distal tubule hypertrophy, elevated renin-Ang II, and aldosterone levels (6). 4) The reduced K ϩ secretion in Romk null mice is compensated by increased maxi-K channel activity in the collecting tubule (7).However, three ROMK isoforms (ROMK1, -2, and -3) have been identified in the rat kidney (8 -10), but unique functions of any of the ROMK isoforms in nephron segments are still poorly understood. ROMK1 is expressed in the distal and collecting tubules and uniquely regulated by PTK/PTP-dependent endocytosis, which may be the mechanism for high-K-mediated enhanced ROMK channel activity in the collecting tubule (11,12). To study the functional role of ROMK1 in the regulation of Na and K homeostasis, we have generated a mouse deficient only in Romk1 by selective deletion of the Romk1 exon, using an ES cell Cre-LoxP strategy. We have examined the phenotypes of these mice by metabolic and renal clearance, and examined K channel activities by the patch clamp. The ion transporters, Nkcc2, Ncc, and Romk2, expression were measured by Q-PCR and ROMK localization was examined by immun...

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Section: Discussionsupporting

confidence: 46%

Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion

Dong

Yan

et al. 2016

Journal of Biological Chemistry

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“…20,21 Regulation of the extracellular ionic environment within the taste bud seems to be a key function. 22 Because of their role in terminating synaptic transmission, these cells are considered to play a supporting, glial-like function within the taste bud. 14 Recently, it has been suggested that type I cells may be responsible for the mediation of sodium transduction.…”

Section: Taste Bud Anatomy and Physiologymentioning

confidence: 99%

Taste perception, associated hormonal modulation, and nutrient intake

et al. 2015

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It is well known that taste perception influences food intake. After ingestion, gustatory receptors relay sensory signals to the brain, which segregates, evaluates, and distinguishes the stimuli, leading to the experience known as "flavor." It is well accepted that five taste qualities -sweet, salty, bitter, sour, and umami -can be perceived by animals. In this review, the anatomy and physiology of human taste buds, the hormonal modulation of taste function, the importance of genetic chemosensory variation, and the influence of gustatory functioning on macronutrient selection and eating behavior are discussed. Individual genotypic variation results in specific phenotypes of food preference and nutrient intake. Understanding the role of taste in food selection and ingestive behavior is important for expanding our understanding of the factors involved in body weight maintenance and the risk of chronic diseases including obesity, atherosclerosis, cancer, diabetes, liver disease, and hypertension.

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“…Type I cells, originally defined ultrastructurally as having electron-dense cytoplasm and elongate, pleomorphic nuclei, are believed to have glial-like functions [6]. These cells synthesize and deposit a powerful ecto-ATPase on their surfaces that degrades the transmitter released by other taste cells [7].…”

Section: Anatomy Of Taste Budsmentioning

confidence: 99%

Taste buds as peripheral chemosensory processors

Roper

2013

Seminars in Cell & Developmental Biology

158

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Taste buds are peripheral chemosensory organs situated in the oral cavity. Each taste bud consists of a community of 50–100 cells that interact synaptically during gustatory stimulation. At least three distinct cell types are found in mammalian taste buds – Type I cells, Receptor (Type II) cells, and Presynaptic (Type III) cells. Type I cells appear to be glial-like cells. Receptor cells express G protein-coupled taste receptors for sweet, bitter, or umami compounds. Presynaptic cells transduce acid stimuli (sour taste). Cells that sense salt (NaCl) taste have not yet been confidently identified in terms of these cell types. During gustatory stimulation, taste bud cells secrete synaptic, autocrine, and paracrine transmitters. These transmitters include ATP, acetylcholine (ACh), serotonin (5-HT), norepinephrine (NE), and GABA. Glutamate is an efferent transmitter that stimulates Presynaptic cells to release 5-HT. This chapter discusses these transmitters, which cells release them, the postsynaptic targets for the transmitters, and how cell–cell communication shapes taste bud signaling via these transmitters.

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Inward rectifier channel, ROMK, is localized to the apical tips of glial‐like cells in mouse taste buds

Cited by 7 publications

References 0 publications

Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion

Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion

Taste perception, associated hormonal modulation, and nutrient intake

Taste buds as peripheral chemosensory processors

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