Correction: Chaves et al. Voltage-Gated Proton Channels in the Tree of Life. Biomolecules 2023, 13, 1035

In the original publication [1], there was a discrepancy in the citation order of the references, starting from reference [87]. The “Chaves, G.; Jardin, C.; Franzen, A.; Mahorivska, I.; Musset, B.; Derst, C. Proton channels in molluscs: A new bivalvian-specific minimal HV4 channel. FEBS J. 2023, 290, 3436–3447. https://doi.org/10.1111/febs.16751.” was missing from the reference list and has now been added as reference 126.

A correction has been made to Table 1, where “Hcl” has been modified to “hcl” for the cell type THP-1.

Table 1. H_V1 in human tissue and other mammalian tissue.

Respiratory Burst	Cell Type	Function of HV1	References
Yes	Eosinophil (human) (rodent)	Charge compensation, prevention of cell death.	[10,12,17,36–46]
Yes	Neutrophil (human) PLB-985 (hcl) HL-60 (hcl) K-562 (hcl) Neutrophil (rodent)	Charge compensation, migration, granula release, calcium homeostasis, pH homeostasis, ERK activity, phagosomal pH homeostasis.	[6,8,10,12–15,41,45,47–53]
Yes	Monocyte (human)	Charge compensation.	[54]
Yes, small	Macrophage (human) THP-1 (hcl) Macrophage (mice)	Charge compensation, phagosome acidification.	[52,55,56]
Yes, small	Osteoclast (rodent/Leporidae)	pH homeostasis, charge compensation, ROS production.	[57–61]
Yes, small	Microglia (rodent) Microglia culture (human) BV-2 (rcl) GM1-R1 (rcl) MLS-9 (rcl)	pH homeostasis, charge compensation, ROS production, microglia-astrocyte communication, neuropathic pain promotion, brain damage enhancing, acidosis exacerbation, M2 polarization reduction, demyelination promotion, white matter injuries promotion, secondary spinal cord damage enhancing, neuroinflammation promotion, pyroptosis increase, motor deficit expansion, autophagy increase, M1 polarization promotion in aged mice.	[22,61–77]
Yes	Kupffer cell (mice/rodent)	Glucose metabolism, ROS production suppression, hyperglycaemia, and hyperinsulinemia prevention.	[23]
No	Cardiac fibroblast (human)	pH homeostasis, membrane potential, potentially beneficial in ischemia.	[78]
Yes, small	Dendritic cells (rodent/human)	TLR9 activation.	[28]
No	Sperm cell (human)	Capacitation, acid extrusion.	[32,33,79,80]
Yes	Oocyte (human)	pH homeostasis.	[34]
No	Type 2 alveolar cells (rodent)	pH regulation.	[5,30,47,81–87]
No	Mast cell (mouse)	pH homeostasis.	[88]
Yes, tiny	B cells (human) (rodent) LK35.2 (rodent)	B cell receptor signalling, migration and proliferation enhancing (short isoform).	[26,27,89,90]
No	T cells (human) Jurkat (human) T cells (rodent)	Apoptosis prevention, pH homeostasis, autoimmune disorders prevention.	[29,89,91–93]
No	Cardiomyocytes (canine)	pH homeostasis.	[11]
No	SHG-44 glioma cells (human)	Apoptosis prevention.	[18]
No	Colorectal cancer (human) SW620 (hcl) HT29 (hcl) LS174T (hcl) Colo205 (hcl)	Prevention of cellular acidosis, support of cancer cell metabolism, pH homeostasis, potential biomarker, and drug target.	[19]
No	Basophils (human)	Exocytosis (histamine release), pH homeostasis.	[16,94]
No	Ovary cells (Hamster)	pH homeostasis.	[95]
No	Breast cancer cells (human primary) MDA-BA-231(hcl) MCF-7 (hcl) MDA-MB-468 (hcl) MDA-MB-453 (hcl) T-47D (hcl) SK-BR-3 (hcl)	Tumor growth, metastasis and invasiveness promotion, (expression predicts prognosis of tumor).	[20,21,96]
No	Lung cancer cell A549 (human)	No information.	[97]
No	Prostate cancer cell PC-3 (human)	No information.	[97]
No	Kidney (human) HEK-293	No information.	[97,98]
Yes, small	Nasal epithelium (human primary culture) JME/CF 15 (human) Cystic fibrosis genotype	Airway surface epithelium acidification, proton extrusion.	[99]
Yes, small	Ciliated tracheal cells (human)	NADPH oxidase activity driven proton extrusion.	[31,99]
Yes, small	lung epithelium fetal (human)	DUOX driven proton release, acid extrusion.	[100]
Yes, tiny	Serous gland cell line Calu-3 (human)	Airway surface epithelium acidification, proton extrusion (to a lesser extent than airway epithelium).	[31]
No	Skeletal muscle myocyte (human)	pH homeostasis.	[7]
No	Glioblastoma cell line (human) T98G	Cell’s survival and migration.	[101]
No	Whole heart (rodent)	NOXs transcription and CO2 homeostasis control, electrophysiological remodelling.	[102]
No/Yes	Vascular system, Immune system	Atherosclerosis advancement (hypothetical).	[103]
No/Yes Whole tissue	Lung (rodent)	Goblet cell hyperplasia prevention. Depression expression of IL-4, IL-5, and IL-13. Reduction of the expression levels of NOX2, NOX4, and DUOX1. Promotion of the expression of SOD2 and catalase. Reduction of the development of allergic asthma through ROS production enhancing.	[104]
Yes	Myeloid derived suppressor cells (MDSC) (rodent)	T-cells regulation (via ROS production).	[35]
No	epididymal adipose tissue (rodent)	Diet obesity induction.	[24]
Yes, tiny	Pancreatic β cells (rodent)	Insulin secretion, ROS production, NOX4 upregulation, glucotoxicity induction.	[25,105,106]

hcl = human cell line; rcl = rodent cell line.

Table 1. H_V1 in human tissue and other mammalian tissue.

Respiratory Burst	Cell Type	Function of HV1	References
Yes	Eosinophil (human) (rodent)	Charge compensation, prevention of cell death.	[10,12,17,36–46]
Yes	Neutrophil (human) PLB-985 (hcl) HL-60 (hcl) K-562 (hcl) Neutrophil (rodent)	Charge compensation, migration, granula release, calcium homeostasis, pH homeostasis, ERK activity, phagosomal pH homeostasis.	[6,8,10,12–15,41,45,47–53]
Yes	Monocyte (human)	Charge compensation.	[54]
Yes, small	Macrophage (human) THP-1 (hcl) Macrophage (mice)	Charge compensation, phagosome acidification.	[52,55,56]
Yes, small	Osteoclast (rodent/Leporidae)	pH homeostasis, charge compensation, ROS production.	[57–61]
Yes, small	Microglia (rodent) Microglia culture (human) BV-2 (rcl) GM1-R1 (rcl) MLS-9 (rcl)	pH homeostasis, charge compensation, ROS production, microglia-astrocyte communication, neuropathic pain promotion, brain damage enhancing, acidosis exacerbation, M2 polarization reduction, demyelination promotion, white matter injuries promotion, secondary spinal cord damage enhancing, neuroinflammation promotion, pyroptosis increase, motor deficit expansion, autophagy increase, M1 polarization promotion in aged mice.	[22,61–77]
Yes	Kupffer cell (mice/rodent)	Glucose metabolism, ROS production suppression, hyperglycaemia, and hyperinsulinemia prevention.	[23]
No	Cardiac fibroblast (human)	pH homeostasis, membrane potential, potentially beneficial in ischemia.	[78]
Yes, small	Dendritic cells (rodent/human)	TLR9 activation.	[28]
No	Sperm cell (human)	Capacitation, acid extrusion.	[32,33,79,80]
Yes	Oocyte (human)	pH homeostasis.	[34]
No	Type 2 alveolar cells (rodent)	pH regulation.	[5,30,47,81–87]
No	Mast cell (mouse)	pH homeostasis.	[88]
Yes, tiny	B cells (human) (rodent) LK35.2 (rodent)	B cell receptor signalling, migration and proliferation enhancing (short isoform).	[26,27,89,90]
No	T cells (human) Jurkat (human) T cells (rodent)	Apoptosis prevention, pH homeostasis, autoimmune disorders prevention.	[29,89,91–93]
No	Cardiomyocytes (canine)	pH homeostasis.	[11]
No	SHG-44 glioma cells (human)	Apoptosis prevention.	[18]
No	Colorectal cancer (human) SW620 (hcl) HT29 (hcl) LS174T (hcl) Colo205 (hcl)	Prevention of cellular acidosis, support of cancer cell metabolism, pH homeostasis, potential biomarker, and drug target.	[19]
No	Basophils (human)	Exocytosis (histamine release), pH homeostasis.	[16,94]
No	Ovary cells (Hamster)	pH homeostasis.	[95]
No	Breast cancer cells (human primary) MDA-BA-231(hcl) MCF-7 (hcl) MDA-MB-468 (hcl) MDA-MB-453 (hcl) T-47D (hcl) SK-BR-3 (hcl)	Tumor growth, metastasis and invasiveness promotion, (expression predicts prognosis of tumor).	[20,21,96]
No	Lung cancer cell A549 (human)	No information.	[97]
No	Prostate cancer cell PC-3 (human)	No information.	[97]
No	Kidney (human) HEK-293	No information.	[97,98]
Yes, small	Nasal epithelium (human primary culture) JME/CF 15 (human) Cystic fibrosis genotype	Airway surface epithelium acidification, proton extrusion.	[99]
Yes, small	Ciliated tracheal cells (human)	NADPH oxidase activity driven proton extrusion.	[31,99]
Yes, small	lung epithelium fetal (human)	DUOX driven proton release, acid extrusion.	[100]
Yes, tiny	Serous gland cell line Calu-3 (human)	Airway surface epithelium acidification, proton extrusion (to a lesser extent than airway epithelium).	[31]
No	Skeletal muscle myocyte (human)	pH homeostasis.	[7]
No	Glioblastoma cell line (human) T98G	Cell’s survival and migration.	[101]
No	Whole heart (rodent)	NOXs transcription and CO2 homeostasis control, electrophysiological remodelling.	[102]
No/Yes	Vascular system, Immune system	Atherosclerosis advancement (hypothetical).	[103]
No/Yes Whole tissue	Lung (rodent)	Goblet cell hyperplasia prevention. Depression expression of IL-4, IL-5, and IL-13. Reduction of the expression levels of NOX2, NOX4, and DUOX1. Promotion of the expression of SOD2 and catalase. Reduction of the development of allergic asthma through ROS production enhancing.	[104]
Yes	Myeloid derived suppressor cells (MDSC) (rodent)	T-cells regulation (via ROS production).	[35]
No	epididymal adipose tissue (rodent)	Diet obesity induction.	[24]
Yes, tiny	Pancreatic β cells (rodent)	Insulin secretion, ROS production, NOX4 upregulation, glucotoxicity induction.	[25,105,106]

hcl = human cell line; rcl = rodent cell line.

In Table 4, letter designations for “a,b,c,e,c” were incorrectly assigned. These designations have been corrected throughout the table to ensure proper attribution.

Table 4. Biophysical properties of some H_V channels.

Organism	Species	Channel	Oligomerization?	Selectivity	Gating Charges, e0	Slope Vthres/Vrev	Vthres at ΔpH = 0 (mV)	ΔgH-V/ΔpH (mV/pHo)	H+ Influx at Relevant Physiological pH?	References
Mammals	H. sapiens	hHV1	confirmed f,g,j,k	>106 PH+/PTMA+ e,i >106 PH+/PCH3SO3- i >106 PH+/PCl- i	~5 h,δ ~6 l	0.82 e 0.67–0.71 (expressed) l 0.71 (native) l	13.8 e −9 to −11 (expressed) l +27 (native) l	40 l	no (native) yes (if expressed) l	[111] e, [139] f, [140] g, [141] h, [142] i, [41] j, [143] k, [98] l
	M. musculus	mHV1	confirmed n	>107 PH+/PNMDG+ >107 PH+/PNa+ >107 PH+/PK+	~6 m	0.86 * (expressed) 0.69 m (expressed)	+10 to +20 −15 (expressed) m	50 40 m	no (native) yes (if expressed) m	[119], [98] m, [144] n
	R. norvegicus	RnHV1	possibly	>107 PH+/PTMA+ o >108 PD+/PTMA+ p	5.4 p	0.76	+18	44 40 o,p	no	[5], [81] o, [83] p
Fish	D. rerio	DrHV1	possibly	>107 PH+/PNMDG+	n.d.	0.69 *	~+10 mV ε	~40 ε	no	[145]
Sea squirt	C. intestinalis	CiHV1	confirmed c	n.d.	4.4–5.9 (dimer) c 1.6–2.7 (monomer) d	n.d.	n.d.	~40 d	no	[119], [146] c, [147] d
Insects	N. phytophila	NpHV1	confirmed b	>108 PH+/PTMA+ >104 PH+/PNa+ >104 PH+/PCl-	4.7–6.1 b	0.81 a	−3.4 a	47–54 a	no	[121] a, [148] b
	E. tiaratum	EtHV1	n.d.	>106 PH+/PTMA+	n.d.	0.77	−23	45	yes	[122]
Mollusks	C. gigas	CgHV4	possibly	>107 PH+/PTMA+	n.d.	0.84	−12	49	no ●	[126]
	A. californica	AcHV1	possibly	>107 PH+/PTMA+ >106 PH+/PNa+ >106 PH+/PK+	5.7	0.78	5	43–45	no	[125]
	A. californica	AcHV2	possibly	>107 PH+/PTMA+ >106 PH+/PK+	5.3	0.77	−20	44 40 (pHi)	yes	[125]
	A. californica	AcHV3	possibly +	>107 PH+/PTMA+	n.d.	n.d.	n.d.	n.d.	yes §	[125]
	H. trivolvis	HtHV1	possibly	>107 PH+/PTMA+	5.5	1.03 * 0.26 (pHi) *	n.d.	60.0 15.3 (pHi)	no	[149]
Corals	A. millepora	AmHV1	confirmed	>107 PH+/PTMA+	2 λ	0.86 *	~+10 mV θ	~50 θ	no	[124]
Sea Urchin	S. purpuratus	SpHV1	confirmed	>107 PH+/PK+	4.3 (dimer) 1.1 (monomer)	0.69 *	~+10 mV	~40 β	no	[123]
Fungi	A. oryzae	AoHV1	possibly +	>105 PH+/PTEA+ #	5	1.40–1.55 *	~−30 (pH 5.5) γ ~−30 (pH 6.5) γ	80–90	yes	[130]
	S. luteus	SlHV1	possibly +	>105 PH+/PTEA+ #	5	1.40–1.55 *	~+20 (pH 5.5) γ ~+40 (pH 6.5) γ	80–90	no	[130]
Dinoflagellates	K. veneficum	kHV1	possibly not φ	>107 PH+/PTMA+ >105 PH+/PCl-	n.d.	0.79	−37	46	yes	[133]
	L. polyedrum	LpHV1	possibly +	>109 PH+/PTMA+	n.d.	0.69 *	46	40 **	yes α	[134]
Phytoplankton	E. huxleyi	EhHV1	possibly	>106 PH+/PK+ >106 PH+/PCl-	n.d.	0.69 μ (expressed)	~+20 mV (expressed) μ	~40 Ω	no	[132]
	C. pelagicus	CpHV1	possibly	>106 PH+/PK+ >106 PH+/PCl-	n.d.	0.69 μ (native)	+10 mV (native) μ	~40 Ω	no	[132]

* Calculated from conductance shifts (∆g_H-V/∆pH) and E_H = 58 mV·pH⁻¹. ^§ AcH_V3 leaks protons at the closed state [125]. ^# Calculated from pH = 6.0 and working solution containing 30 mM of TEA⁺ as main cation. ^● CgH_V4 has an activation of −12 mV which permits proton influx at symmetrical pH (physiological) conditions. Nevertheless, the proximity of the offset value to V_rev makes the inward H⁺ electrochemical gradient small. Thus, H⁺ influx is small at ∆pH = 0 where currents rectify rapidly with depolarization, behaving more like a typical H_V proton extruder. During measurements, strong and/or consistent H⁺ influx currents were not detected. ^φ kH_V1 lacks the predicted coiled-coil which is important for H_V dimerization, a potential monomeric expression is discussed by the authors [133]. ⁺ Protein sequence analysis predicts a C-terminal coiled-coil domain. ** LpH_V1 pH-dependent gating saturates above pH_o 8.0 [134] similar to rat, human, Karlodinium, and Emiliania H_V channels [137]. ^α Inward H⁺ currents are onset at large inward pH gradients (1–3 ∆pH units) [134]. ^β estimated from g_H-V curves shift between pH_o 6.5 and 7.0 (~20 mV), at pH_i = 7.0 (Figure 2; [123]). The g_H-V shifts between pH_o 6.0 to 6.5 and 6.5 to 7.0 are not identical due to experimental limitations reported by the authors. The calculated value on pH_o-dependent gating agrees with Δg_H-V/pH_i unit (Figure S1; [123]). ^γ from normalized g_H-V curves (Figure 3; [130]). ^δ from Q_on of dimeric W207A-N214R mutant ([141]). ^θ from V_thres-ΔpH and slope of V_0.5-ΔpH curves (Figure 6; [124]). ^λ apparent from steepness of normalized g_H-V (Figure 6; [124]). ^Ω from current densities (Figure 1; [132]). ^μ the slope V_thres/V_rev was calculated from shifts of I_H onsets and E_H. V_offset was estimated shifts of I_H activation, E_H, and Equation (3) (Figure 4; [132]). P_H+ = proton permeability, P_TMA+ = tetramethylammonium permeability, P_TEA+ = tetraethylammonium permeability, P_K+ = potassium permeability, P_Na+ = sodium permeability, P_Cl- = chloride permeability, P_NMDG+ = N-methyl-d-glucamine permeability, P_CH3SO3-= methanesulfonate permeability, n.d. = no data, V_thres = threshold potential, V_rev = reversal potential, ∆pH = proton gradient (pH_outside – pH_inside), g_H-V = proton conductance – voltage relationship, pH_o = external pH, pH_i = internal pH.

Table 4. Biophysical properties of some H_V channels.

Organism	Species	Channel	Oligomerization?	Selectivity	Gating Charges, e0	Slope Vthres/Vrev	Vthres at ΔpH = 0 (mV)	ΔgH-V/ΔpH (mV/pHo)	H+ Influx at Relevant Physiological pH?	References
Mammals	H. sapiens	hHV1	confirmed f,g,j,k	>106 PH+/PTMA+ e,i >106 PH+/PCH3SO3- i >106 PH+/PCl- i	~5 h,δ ~6 l	0.82 e 0.67–0.71 (expressed) l 0.71 (native) l	13.8 e −9 to −11 (expressed) l +27 (native) l	40 l	no (native) yes (if expressed) l	[111] e, [139] f, [140] g, [141] h, [142] i, [41] j, [143] k, [98] l
	M. musculus	mHV1	confirmed n	>107 PH+/PNMDG+ >107 PH+/PNa+ >107 PH+/PK+	~6 m	0.86 * (expressed) 0.69 m (expressed)	+10 to +20 −15 (expressed) m	50 40 m	no (native) yes (if expressed) m	[119], [98] m, [144] n
	R. norvegicus	RnHV1	possibly	>107 PH+/PTMA+ o >108 PD+/PTMA+ p	5.4 p	0.76	+18	44 40 o,p	no	[5], [81] o, [83] p
Fish	D. rerio	DrHV1	possibly	>107 PH+/PNMDG+	n.d.	0.69 *	~+10 mV ε	~40 ε	no	[145]
Sea squirt	C. intestinalis	CiHV1	confirmed c	n.d.	4.4–5.9 (dimer) c 1.6–2.7 (monomer) d	n.d.	n.d.	~40 d	no	[119], [146] c, [147] d
Insects	N. phytophila	NpHV1	confirmed b	>108 PH+/PTMA+ >104 PH+/PNa+ >104 PH+/PCl-	4.7–6.1 b	0.81 a	−3.4 a	47–54 a	no	[121] a, [148] b
	E. tiaratum	EtHV1	n.d.	>106 PH+/PTMA+	n.d.	0.77	−23	45	yes	[122]
Mollusks	C. gigas	CgHV4	possibly	>107 PH+/PTMA+	n.d.	0.84	−12	49	no ●	[126]
	A. californica	AcHV1	possibly	>107 PH+/PTMA+ >106 PH+/PNa+ >106 PH+/PK+	5.7	0.78	5	43–45	no	[125]
	A. californica	AcHV2	possibly	>107 PH+/PTMA+ >106 PH+/PK+	5.3	0.77	−20	44 40 (pHi)	yes	[125]
	A. californica	AcHV3	possibly +	>107 PH+/PTMA+	n.d.	n.d.	n.d.	n.d.	yes §	[125]
	H. trivolvis	HtHV1	possibly	>107 PH+/PTMA+	5.5	1.03 * 0.26 (pHi) *	n.d.	60.0 15.3 (pHi)	no	[149]
Corals	A. millepora	AmHV1	confirmed	>107 PH+/PTMA+	2 λ	0.86 *	~+10 mV θ	~50 θ	no	[124]
Sea Urchin	S. purpuratus	SpHV1	confirmed	>107 PH+/PK+	4.3 (dimer) 1.1 (monomer)	0.69 *	~+10 mV	~40 β	no	[123]
Fungi	A. oryzae	AoHV1	possibly +	>105 PH+/PTEA+ #	5	1.40–1.55 *	~−30 (pH 5.5) γ ~−30 (pH 6.5) γ	80–90	yes	[130]
	S. luteus	SlHV1	possibly +	>105 PH+/PTEA+ #	5	1.40–1.55 *	~+20 (pH 5.5) γ ~+40 (pH 6.5) γ	80–90	no	[130]
Dinoflagellates	K. veneficum	kHV1	possibly not φ	>107 PH+/PTMA+ >105 PH+/PCl-	n.d.	0.79	−37	46	yes	[133]
	L. polyedrum	LpHV1	possibly +	>109 PH+/PTMA+	n.d.	0.69 *	46	40 **	yes α	[134]
Phytoplankton	E. huxleyi	EhHV1	possibly	>106 PH+/PK+ >106 PH+/PCl-	n.d.	0.69 μ (expressed)	~+20 mV (expressed) μ	~40 Ω	no	[132]
	C. pelagicus	CpHV1	possibly	>106 PH+/PK+ >106 PH+/PCl-	n.d.	0.69 μ (native)	+10 mV (native) μ	~40 Ω	no	[132]

* Calculated from conductance shifts (∆g_H-V/∆pH) and E_H = 58 mV·pH⁻¹. ^§ AcH_V3 leaks protons at the closed state [125]. ^# Calculated from pH = 6.0 and working solution containing 30 mM of TEA⁺ as main cation. ^● CgH_V4 has an activation of −12 mV which permits proton influx at symmetrical pH (physiological) conditions. Nevertheless, the proximity of the offset value to V_rev makes the inward H⁺ electrochemical gradient small. Thus, H⁺ influx is small at ∆pH = 0 where currents rectify rapidly with depolarization, behaving more like a typical H_V proton extruder. During measurements, strong and/or consistent H⁺ influx currents were not detected. ^φ kH_V1 lacks the predicted coiled-coil which is important for H_V dimerization, a potential monomeric expression is discussed by the authors [133]. ⁺ Protein sequence analysis predicts a C-terminal coiled-coil domain. ** LpH_V1 pH-dependent gating saturates above pH_o 8.0 [134] similar to rat, human, Karlodinium, and Emiliania H_V channels [137]. ^α Inward H⁺ currents are onset at large inward pH gradients (1–3 ∆pH units) [134]. ^β estimated from g_H-V curves shift between pH_o 6.5 and 7.0 (~20 mV), at pH_i = 7.0 (Figure 2; [123]). The g_H-V shifts between pH_o 6.0 to 6.5 and 6.5 to 7.0 are not identical due to experimental limitations reported by the authors. The calculated value on pH_o-dependent gating agrees with Δg_H-V/pH_i unit (Figure S1; [123]). ^γ from normalized g_H-V curves (Figure 3; [130]). ^δ from Q_on of dimeric W207A-N214R mutant ([141]). ^θ from V_thres-ΔpH and slope of V_0.5-ΔpH curves (Figure 6; [124]). ^λ apparent from steepness of normalized g_H-V (Figure 6; [124]). ^Ω from current densities (Figure 1; [132]). ^μ the slope V_thres/V_rev was calculated from shifts of I_H onsets and E_H. V_offset was estimated shifts of I_H activation, E_H, and Equation (3) (Figure 4; [132]). P_H+ = proton permeability, P_TMA+ = tetramethylammonium permeability, P_TEA+ = tetraethylammonium permeability, P_K+ = potassium permeability, P_Na+ = sodium permeability, P_Cl- = chloride permeability, P_NMDG+ = N-methyl-d-glucamine permeability, P_CH3SO3-= methanesulfonate permeability, n.d. = no data, V_thres = threshold potential, V_rev = reversal potential, ∆pH = proton gradient (pH_outside – pH_inside), g_H-V = proton conductance – voltage relationship, pH_o = external pH, pH_i = internal pH.

Additionally, several textual clarifications have been made: the term “putatively” was added to qualify the described mechanism, the phrase “translate to” was introduced to improve the accuracy of the affected sentence, and the repeated year “2006” in the description of the Ciona intestinalis homolog was removed.

With this correction, the order of some references has been adjusted accordingly. The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.