Focal adhesion kinase and β1 integrin regulation of Na+, K+, 2Cl− cotransporter in osmosensing ion transporting cells of killifish, Fundulus heteroclitus

Marshall, William S.; Katoh, Fumi; Main, Heather; Sers, N.; Cozzi, Regina R. F.

doi:10.1016/j.cbpa.2008.03.013

Cited by 28 publications

(21 citation statements)

References 54 publications

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“…However, only FAK pY407 immunogold particles were present throughout the basolateral membrane (Fig. 2E), a confirmation of previous immunoelectron microscopy findings (Marshall et al, 2008). Interestingly, FAK pY407 was also detected in the pavement cells (Fig.…”

Section: Cftr and Fak Py407 Distribution In Isotonic Conditionssupporting

confidence: 90%

“…In previous immunocytochemical experiments we discovered a novel association of CFTR and the tyrosine kinase FAK (Marshall et al, 2008). Using phosphorylation specific antibodies directed to conserved tyrosine phosphorylation sites on FAK, we localized FAK pY407 and colocalized FAK pY576 with CFTR in the apical membranes of MR cells (Marshall et al, 2008). Furthermore, we observed that other stimuli that inhibit Cl -secretion by the MR cells also dephosphorylate FAK pY407, thus preventing FAK immunostaining at pY407 (Marshall et al, 2008).…”

Section: Introductionmentioning

confidence: 69%

Section: Introductionmentioning

confidence: 83%

“…Using phosphorylation specific antibodies directed to conserved tyrosine phosphorylation sites on FAK, we localized FAK pY407 and colocalized FAK pY576 with CFTR in the apical membranes of MR cells (Marshall et al, 2008). Furthermore, we observed that other stimuli that inhibit Cl -secretion by the MR cells also dephosphorylate FAK pY407, thus preventing FAK immunostaining at pY407 (Marshall et al, 2008). Hence, there is a potential functional relationship between CFTR and FAK in the apical membrane of MR cells.…”

Section: Introductionmentioning

confidence: 83%

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CFTR Cl– channel functional regulation by phosphorylation of focal adhesion kinase at tyrosine 407 in osmosensitive ion transporting mitochondria rich cells of euryhaline killifish

Marshall

Watters

Hovdestad

et al. 2009

Journal of Experimental Biology

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SUMMARYCystic fibrosis transmembrane conductance regulator (CFTR) anion channels are the regulated exit pathway in Cl -secretion by teleost mitochondria rich salt secreting (MR) cells of the gill and opercular epithelia of euryhaline teleosts. By confocal light immunocytochemistry, immunogold transmission electron microscopy (TEM), and co-immunoprecipitation, using regular and phospho-antibodies directed against conserved sites, we found that killifish CFTR (kfCFTR) and the tyrosine kinase focal adhesion kinase (FAK) phosphorylated at Y407 (FAK pY407) are colocalized in the apical membrane and in subjacent membrane vesicles of MR cells. We showed previously that basolateral FAK pY407, unlike other FAK phosphorylation sites, is osmosensitive and dephosphorylates during hypotonic shock of epithelial cells (Marshall et al., 2008). In the present study, we found that hypotonic shock and the α 2 -adrenergic agonist clonidine (neither of which affects cAMP levels) rapidly and reversibly inhibit Cl -secretion by isolated opercular membranes, simultaneous with dephosphorylation of FAK pY407, located in the apical membrane. FAK pY407 is rephosphorylated and Cl -secretion rapidly restored by hypertonic shock as well as by forskolin and isoproterenol, which operate via cAMP and protein kinase A. We conclude that hormone mediated, cAMP dependent and osmotically mediated, cAMP independent pathways converge on a mechanism to activate CFTR and Cl -secretion, possibly through tyrosine phosphorylation of CFTR by FAK.

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Section: Cftr and Fak Py407 Distribution In Isotonic Conditionssupporting

confidence: 90%

Section: Introductionmentioning

confidence: 69%

Section: Introductionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 83%

See 2 more Smart Citations

CFTR Cl– channel functional regulation by phosphorylation of focal adhesion kinase at tyrosine 407 in osmosensitive ion transporting mitochondria rich cells of euryhaline killifish

Marshall

Watters

Hovdestad

et al. 2009

Journal of Experimental Biology

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“…Moreover, focal adhesion kinase (FAK) is dephosphorylated in response to hypo-osmotic stress in killifish gill and opercular epithelia (Marshall et al, 2005). FAK dephosphorylation has been shown to regulate the activity of Na + /K + /2Cl -co-transporter (NKCC) and cystic fibrosis transmembrane conductance regulator (CTFR) transport proteins during salinity stress (Marshall et al, 2008(Marshall et al, , 2009. Another signaling protein participating in osmosensing in a variety of euryhaline fishes is osmotic stress transcription factor 1 (OSTF1), which may have a role in governing changes in expression of ion transporters and channels (Fiol and Kültz, 2005;Fiol et al, 2006;Choi and An, 2008;Tse et al, 2008;Breves et al, 2010;McGuire et al, 2010).…”

Section: Evolution Of High Salinity Tolerance In Euryhaline Fishesmentioning

confidence: 99%

Physiological mechanisms used by fish to cope with salinity stress

Kültz

2015

Journal of Experimental Biology

325

161

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Salinity represents a critical environmental factor for all aquatic organisms, including fishes. Environments of stable salinity are inhabited by stenohaline fishes having narrow salinity tolerance ranges. Environments of variable salinity are inhabited by euryhaline fishes having wide salinity tolerance ranges. Euryhaline fishes harbor mechanisms that control dynamic changes in osmoregulatory strategy from active salt absorption to salt secretion and from water excretion to water retention. These mechanisms of dynamic control of osmoregulatory strategy include the ability to perceive changes in environmental salinity that perturb body water and salt homeostasis (osmosensing), signaling networks that encode information about the direction and magnitude of salinity change, and epithelial transport and permeability effectors. These mechanisms of euryhalinity likely arose by mosaic evolution involving ancestral and derived protein functions. Most proteins necessary for euryhalinity are also critical for other biological functions and are preserved even in stenohaline fish. Only a few proteins have evolved functions specific to euryhaline fish and they may vary in different fish taxa because of multiple independent phylogenetic origins of euryhalinity in fish. Moreover, proteins involved in combinatorial osmosensing are likely interchangeable. Most euryhaline fishes have an upper salinity tolerance limit of approximately 2× seawater (60 g kg −1). However, some species tolerate up to 130 g kg −1 salinity and they may be able to do so by switching their adaptive strategy when the salinity exceeds 60 g kg −1. The superior salinity stress tolerance of euryhaline fishes represents an evolutionary advantage favoring their expansion and adaptive radiation in a climate of rapidly changing and pulsatory fluctuating salinity. Because such a climate scenario has been predicted, it is intriguing to mechanistically understand euryhalinity and how this complex physiological phenotype evolves under high selection pressure.

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Volume Regulation in Epithelia

Larsen

Hoffmann

2015

Ion Channels and Transporters of Epithelia in Health and Disease

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Focal adhesion kinase and β1 integrin regulation of Na+, K+, 2Cl− cotransporter in osmosensing ion transporting cells of killifish, Fundulus heteroclitus

Cited by 28 publications

References 54 publications

CFTR Cl– channel functional regulation by phosphorylation of focal adhesion kinase at tyrosine 407 in osmosensitive ion transporting mitochondria rich cells of euryhaline killifish

CFTR Cl– channel functional regulation by phosphorylation of focal adhesion kinase at tyrosine 407 in osmosensitive ion transporting mitochondria rich cells of euryhaline killifish

Physiological mechanisms used by fish to cope with salinity stress

Volume Regulation in Epithelia

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