Molecular genetics of coat colour variations in White Galloway and White Park cattle

White Galloway cattle exhibit three different white coat colour phenotypes, that is, well marked, strongly marked and mismarked. However, mating of individuals with the preferred well or strongly marked phenotype also results in offspring with the undesired mismarked and/or even fully black coat colour. To elucidate the genetic background of the coat colour variations in White Galloway cattle, we analysed four coat colour relevant genes: mast/stem cell growth factor receptor (KIT), KIT ligand (KITLG), melanocortin 1 receptor (MC1R) and tyrosinase (TYR). Here, we show that the coat colour variations in White Galloway cattle and White Park cattle are caused by a KIT gene (chromosome 6) duplication and aberrant insertion on chromosome 29 (Cs₂₉) as recently described for colour‐sided Belgian Blue. Homozygous (Cs₂₉/Cs₂₉) White Galloway cattle and White Park cattle exhibit the mismarked phenotype, whereas heterozygous (Cs₂₉/wt₂₉) individuals are either well or strongly marked. In contrast, fully black individuals are characterised by the wild‐type chromosome 29. As known for other cattle breeds, mutations in the MC1R gene determine the red colouring. Our data suggest that the white coat colour variations in White Galloway cattle and White Park cattle are caused by a dose‐dependent effect based on the ploidy of aberrant insertions and inheritance of the KIT gene on chromosome 29.     

A complex structural variant at the KIT locus in cattle with the Pinzgauer spotting pattern

A specific white spotting phenotype, termed finching or line‐backed spotting, is known for all Pinzgauer cattle and occurs occasionally in Tux‐Zillertaler cattle, two Austrian breeds. The so‐called Pinzgauer spotting is inherited as an autosomal incompletely dominant trait. A genome‐wide association study using 27 white spotted and 16 solid‐coloured Tux‐Zillertaler cattle, based on 777k SNP data, revealed a strong signal on chromosome 6 at the KIT locus. Haplotype analyses defined a critical interval of 122 kb downstream of the KIT coding region. Whole‐genome sequencing of a Pinzgauer cattle and comparison to 338 control genomes revealed a complex structural variant consisting of a 9.4‐kb deletion and an inversely inserted duplication of 1.5 kb fused to a 310‐kb duplicated segment from chromosome 4. A diagnostic PCR was developed for straightforward genotyping of carriers for this structural variant (KIT^PINZ) and confirmed that the variant allele was present in all Pinzgauer and most of the white spotted Tux‐Zillertaler cattle. In addition, we detected the variant in all Slovenian Cika, British Gloucester and Spanish Berrenda en negro cattle with similar spotting patterns. Interestingly, the KIT^PINZ variant occurs in some white spotted animals of the Swiss breeds Evolèner and Eringer. The introgression of the KIT^PINZ variant confirms admixture and the reported historical relationship of these short‐headed breeds with Austrian Tux‐Zillertaler and suggests a mutation event, occurring before breed formation.     

The genetics of brown coat color and white spotting in domestic yaks (Bos grunniens)

Domestic yaks (Bos grunniens) exhibit two major coat color variations: a brown vs. wild‐type black pigmentation and a white spotting vs. wild‐type solid color pattern. The genetic basis for these variations in color and distribution remains largely unknown and may be complicated by a breeding history involving hybridization between yaks and cattle. Here, we investigated 92 domestic yaks from China using a candidate gene approach. Sequence variations in MC1R, PMEL and TYRP1 were surveyed in brown yaks; TYRP1 was unassociated with the coloration and excluded. Recessive mutations from MC1R, or p.Gln34*, p.Met73Leu and possibly p.Arg142Pro, are reported in bovids for the first time and accounted for approximately 40% of the brown yaks in this study. The remaining 60% of brown individuals correlated with a cattle‐derived deletion mutation from PMEL (p.Leu18del) in a dominant manner. Degrees of white spotting found in yaks vary from color sidedness and white face, to completely white. After examining the candidate gene KIT, we suggest that color‐sided and all‐white yaks are caused by the serial translations of KIT (Cs₆ or Cs₂₉) as reported for cattle. The white‐faced phenotype in yaks is associated with the KIT haplotype S^wf. All KIT mutations underlying the serial phenotypes of white spotting in yaks are identical to those in cattle, indicating that cattle are the likely source of white spotting in yaks. Our results reveal the complex genetic origins of domestic yak coat color as either native in yaks through evolution and domestication or as introduced from cattle through interspecific hybridization.     

A de novo germline mutation of KIT in a white-spotted Brown Swiss cow

White-spotting coat colour phenotypes in cattle are either fixed characteristics of specific cattle breeds or occur sporadically owing to germline genetic variation of solid-coloured parents. A Brown Swiss cow showing a piebald pattern resembling colour-sidedness was referred for genetic evaluation. Both parents were normal solid-brown-coloured cattle. The cow was tested negative for the three known DNA variants in KIT, MITF and TWIST2 associated with different depigmentation phenotypes in Brown Swiss cattle. Whole-genome sequencing of the cow was performed and a heterozygous variant affecting the coding sequence of the bovine KIT gene was identified on chromosome 6. The variant is a 40 bp deletion in exon 9, NM_001166484.1:c.1390_1429del, and leads to a frameshift that is predicted to produce a novel 50 amino acid-long C-terminus replacing almost 50% of the wt KIT protein, including the functionally important intracellular tyrosine kinase domain (NP_001159956.1:p.(Asn464AlafsTer50)). Interestingly, among three available offspring, two solid-coloured daughters were genotyped as homozygous wt whereas a single son showing a slightly milder but still obvious depigmentation phenotype inherited a copy of the novel variant allele. The genetic findings provide strong evidence that the identified loss-of-function KIT variant most likely represents a de novo germline mutation that is causative owing to haploinsufficiency.     

Genetic heterogeneity at the bovine KIT gene in cattle breeds carrying different putative alleles at the spotting locus

According to classical genetic studies, piebaldism in cattle is largely influenced by the allelic series at the spotting locus (S), which includes the S^H (Hereford pattern), S⁺ (non‐spotted) and s (spotted) alleles. The S locus was mapped on bovine chromosome 6 in the region containing the KIT gene. We investigated the KIT gene, analysing its variability and haplotype distribution in cattle of three breeds (Angus, Hereford and Holstein) with different putative alleles (S⁺, S^H and s respectively) at the S locus. Resequencing of a whole of 0.485 Mb revealed 111 polymorphisms. The global nucleotide diversity was 0.087%. Tajima’s D‐values were negative for all breeds, indicating putative directional selection. Of the 28 inferred haplotypes, only five were observed in the Hereford breed, in which one was the most frequent. Coalescent simulation showed that it is highly unlikely (P < 10E‐6) to obtain this low number of haplotypes conditionally on the observed number of segregating SNPs. Therefore, the neutral model could be rejected for the Hereford breed, suggesting that a selection sweep occurred at the KIT locus. Twelve haplotypes were inferred in Holstein and Angus. For these two breeds, the neutral model could not be rejected. High heterogeneity of the KIT gene was confirmed from a phylogenetic analysis. Our results suggest a role of the KIT gene in determining the S^H allele(s) in the Hereford, but no evidence of selective sweep was obtained in Holstein, suggesting that complex mechanisms (or other genes) might be the cause of the spotted phenotype in this breed.     

A novel KIT deletion variant in a German Riding Pony with white‐spotting coat colour phenotype

White spotting phenotypes in horses may be caused by developmental alterations impairing melanoblast differentiation, survival, migration and/or proliferation. Candidate genes for white‐spotting phenotypes in horses include EDNRB, KIT, MITF, PAX3 and TRPM1. We investigated a German Riding Pony with a sabino‐like phenotype involving extensive white spots on the body together with large white markings on the head and almost completely white legs. We obtained whole genome sequence data from this horse. The analysis revealed a heterozygous 1273‐bp deletion spanning parts of intron 2 and exon 3 of the equine KIT gene (Chr3: 79 579 925–79 581 197). We confirmed the breakpoints of the deletion by PCR and Sanger sequencing. Knowledge of the functional impact of similar KIT variants in horses and other species suggests that this deletion represents a plausible candidate causative variant for the white‐spotting phenotype. We propose the designation W28 for the mutant allele.     

Involvement of oxidative stress in hydroquinone-induced cytotoxicity in catalase-deficient Escherichia coli mutants

Hydroquinone is a benzene-derived metabolite. To clarify whether the reactive oxygen species (ROS) are involved in hydroquinone-induced cytotoxicity, we constructed transformants of Escherichia coli (E. coli) strains that express mammalian catalase gene derived from catalase mutant mice (Cs^b, Cs^c) and the wild-type (Cs^a) using a catalase-deficient E. coli UM255 as a recipient. Specific catalase activities of these tester strains were in order of Cs^a > Cs^c > Cs^b > UM255, and their susceptibility to hydrogen peroxide (H₂O₂) showed UM255 > Cs^b > Cs^c > Cs^a. We found that hydroquinone exposure reduced the survival of catalase-deficient E. coli mutants in a dose-dependent manner significantly, especially in the strains with lower catalase activities. Hydroquinone toxicity was also confirmed using zone of inhibition test, in which UM255 was the most susceptible, showing the largest zone of growth inhibition, followed by Cs^b, Cs^c and Cs^a. Furthermore, we found that hydroquinone-induced cell damage was inhibited by the pretreatment of catalase, ascorbic acid, dimethyl sulfoxide (DMSO), and ethylenediaminetetraacetic acid (EDTA), and augmented by superoxide dismutase (both CuZnSOD and MnSOD). The present results suggest that H₂O₂ is probably involved in hydroquinone-induced cytotoxicity in catalase-deficient E. coli mutants and catalase plays an important role in protection of the cells against hydroquinone toxicity.     

Anionic polyelectrolyte poly(acrylic acid) (PAA) chain shrinkage in water–ethanol solution in presence of Li+ and Cs+ metal ions studied by molecular dynamics simulations

Molecular dynamic simulations of anionic polyelectrolyte poly(acrylic acid) (PAA) in water–ethanol solution, specifically Li⁺-PAA and Cs⁺-PAA, were carried out across the solvent composition range 0 ≤ ф_eth ≤ 0.9. Chain collapse (i.e. shrinkage) occurs with increase in ф_eth for both types of counter-ion systems and in agreement with the experiments. The qualitative difference in the collapse point is in agreement with experimental results, with counter-ion specific chain collapse of PAA following the order Li⁺ > Cs⁺. With increase in ф_eth the number of hydrogen-bonds between PAA and water decreases while that between PAA and ethanol increases. At higher level of ethanol content in solution, ethanol molecules displace water molecules from the vicinity of the chain. The analysis of the radial distribution functions shows that counter-ion binding distance of Li⁺ to chain is lesser as compared to that of Cs⁺, as well as a higher coordination number exhibited by Li⁺. Thus, as compared to Cs⁺-PAA, greater number of contact ion pairs formed between Li⁺ and PAA induce chain collapse more easily. The coordination of Li⁺ to PAA is better than that of Cs⁺ throughout the ф_eth range, which could be the reason for the greater extent of PAA chain shrinkage observed in the case of Li⁺. Binding of water molecule to PAA units is stronger in the case of Cs⁺. The backbone dihedral trans probability of both systems displayed a decrease with ф_eth indicating chain shrinkage. The relaxation time of H-bonds between PAA and EtOH is greater for Li⁺-PAA as compared to Cs⁺-PAA system. The enhancement of counter-ion pairs formation is found to be directly responsible for the solvent composition at which chain collapse occurs in the particular system.     

Genomic regions influencing coat color saturation and facial markings in Fleckvieh cattle

Genomic regions associated with coat color and pigmented areas of the head were identified for Fleckvieh (dual‐purpose Simmental), a red‐spotted and white‐headed cattle breed. Coat color was measured with a chromameter, implementing the CIELAB color space and resulting in numerical representation of lightness, color intensity, red/green and blue/yellow color components, rather than subjective classification. Single marker regression analyses with fixed effects of the sex and barn were applied, and significant regions were determined with the local false discovery rate methodology. The PMEL and ERBB3 genes on chromosome 5 were in the most significant region for the color measurements. In addition to the blue/yellow color component and color intensity, the AP3B2 gene on chromosome 21 was identified. Its function was confirmed for similar traits in a range of model species. The KIT gene on chromosome 6 was found to be strongly associated with the inhibition of circum‐ocular pigmentation and pigmented spots on the cheek.     

Novel variants in the KIT and PAX3 genes in horses with white‐spotted coat colour phenotypes

Variants in the EDNRB, KIT, MITF, PAX3 and TRPM1 genes are known to cause white spotting phenotypes in horses, which can range from the common white markings up to completely white horses. In this study, we investigated these candidate genes in 169 horses with white spotting phenotypes not explained by the previously described variants. We identified a novel missense variant, PAX3:p.Pro32Arg, in Appaloosa horses with a splashed white phenotype in addition to their leopard complex spotting patterns. We also found three novel variants in the KIT gene. The splice site variant c.1346+1G>A occurred in a Swiss Warmblood horse with a pronounced depigmentation phenotype. The missense variant p.Tyr441Cys was present in several part‐bred Arabians with sabino‐like depigmentation phenotypes. Finally, we provide evidence suggesting that the common and widely distributed KIT:p.Arg682His variant has a very subtle white‐increasing effect, which is much less pronounced than the effect of the other described KIT variants. We termed the new KIT variants W18–W20 to provide a simple and unambiguous nomenclature for future genetic testing applications.     

Pigs with the dominant white coat color phenotype carry a duplication of the KIT gene encoding the mast/stem cell growth factor receptor

Comparative mapping data suggested that the dominant white coat color in pigs may be due to a mutation in KIT which encodes the mast/stem cell growth factor receptor. We report here that dominant white pigs lack melanocytes in the skin, as would be anticipated for a KIT mutation. We found a complete association between the dominant white mutation and a duplication of the KIT gene, or part of it, in samples of unrelated pigs representing six different breeds. The duplication was revealed by single strand conformation polymorphism (SSCP) analysis and subsequent sequence analysis showing that white pigs transmitted two nonallelic KIT sequences. Quantitative Southern blot and quantitative PCR analysis, as well as fluorescence in situ hybridization (FISH) analysis, confirmed the presence of a gene duplication in white pigs. FISH analyses showed that KIT and the very closely linked gene encoding the platelet-derived growth factor receptor (PDGFRA) are both located on the short arm of Chromosome (Chr) 8 at band 8p12. The result revealed an extremely low rate of recombination in the centromeric region of this chromosome, since the closely linked (0.5 cM) serum albumin (ALB) locus has previously been in situ mapped to the long arm (8q12). Pig Chr 8 shares extensive conserved synteny with human Chr 4, but the gene order is rearranged. Received: 22 March 1996 / Accepted: 24 June 1996     

Ion Secretion and Isotonic Transport in Frog Skin Glands

The aim of this study was to clarify the mechanism of isotonic fluid transport in frog skin glands. Stationary ion secretion by the glands was studied by measuring unidirectional fluxes of ²⁴Na⁺, ⁴²K⁺, and carrier-free ¹³⁴Cs⁺ in paired frog skins bathed on both sides with Ringer's solution, and with 10⁻⁵ m noradrenaline on the inside and 10⁻⁴ m amiloride on the outside. At transepithelial thermodynamic equilibrium conditions, the ¹³⁴Cs⁺ flux ratio, J ^out _Cs/J ⁱⁿ _Cs, varied in seven pairs of preparations from 6 to 36. Since carrier-free ¹³⁴Cs⁺ entering the cells is irreversibly trapped in the cellular compartment (Ussing & Lind, 1996), the transepithelial net flux of ¹³⁴Cs⁺ indicates that a paracellular flow of water is dragging ¹³⁴Cs⁺ in the direction from the serosal- to outside solution. From the measured flux ratios it was calculated that the force driving the secretory flux of Cs⁺ varied from 30 to 61 mV among preparations. In the same experiments unidirectional Na⁺ fluxes were measured as well, and it was found that also Na⁺ was subjected to secretion. The ratio of unidirectional Na⁺ fluxes, however, was significantly smaller than would be predicted if the two ions were both flowing along the paracellular route dragged by the flow of water. This result indicates that Na⁺ and Cs⁺ do not take the same pathway through the glands. The flux ratio of unidirectional K⁺ fluxes indicated active secretion of K⁺. The time it takes for steady-state K⁺ fluxes to be established was significantly longer than that of the simultaneously measured Cs⁺ fluxes. These results allow the conclusion that — in addition to being transported between cells — K⁺ is submitted to active transport along a cellular pathway.Based on the recirculation theory, we propose a new model which accounts for stationary Na⁺, K⁺, Cl⁻ and water secretion under thermodynamic equilibrium conditions. The new features of the model, as compared to the classical Silva-model for the shark-rectal gland, are: (i) the sodium pumps in the activated gland transport Na⁺ into the lateral intercellular space only. (ii) A barrier at the level of the basement membrane prevents the major fraction of Na⁺ entering the lateral space from returning to the serosal bath. Thus, Na⁺ is secreted into the outside bath. It has to be assumed then that the Na⁺ permeability of the basement membrane barrier (P ^BM _Na) is smaller than the Na⁺ permeability of the junctional membrane (P ^JM _Na), i.e., P ^JM _Na/P ^BM _Na > 1. The secretory paracellular flow of water further requires that the Na⁺ reflection coefficients (σ_Na) of the two barriers are governed by the conditions, σ^BM _Na > 0, and σ^BM _Na > σ^JM _Na. (iii) Na⁺ channels are located in the apical membrane of the activated gland cells, so that a fraction of the Na⁺ outflux appearing downstream the lateral intercellular space is recirculated by the gland cells. Based on measured unidirectional fluxes, a set of equations is developed from which we estimate the ion fluxes flowing through major pathways during stationary secretion. It is shown that 80% of the sodium ions flowing downstream the lateral intercellular space is recycled by the gland cells. Our calculations also indicate that under the conditions prevailing in the present experiments 1.8 ATP molecule would be hydrolyzed for every Na⁺ secreted to the outside bath. Received: 30 January 1996/Revised: 12 March 1996     

The Belt mutation in pigs is an allele at the Dominant white (I/KIT) locus

A white belt is a common coat color phenotype in pigs and is determined by a dominant allele (Be). Here we present the result of a genome scan performed using a Hampshire (Belt)/Pietrain (non-Belt) backcross segregating for the white belt trait. We demonstrate that Belt maps to the centromeric region of pig Chromosome (Chr) 8 harboring the Dominant white (I/KIT) locus. Complete cosegregation between Belt and a single nucleotide polymorphism in the KIT gene was observed. Another potential candidate gene, the endothelin receptor type A gene (EDNRA), was excluded as it was assigned to a different region (SSC8q21) by FISH analysis. We argue that Belt is a regulatory KIT mutation on the basis of comparative data on mouse KIT mutants and our previous sequence analysis of the KIT coding sequence from a Hampshire pig. Quantitative PCR analysis revealed that Belt is not associated with a KIT duplication, as is the case for the Patch and Dominant white alleles. Thus, Belt is a fourth allele at the Dominant white locus, and we suggest that it is denoted I ^Be . Received: 5 May 1999 / Accepted: 3 August 1999     

Genetic variation at KIT locus may predispose to melanoma

As loss of KIT frequently occurs in melanoma progression, we hypothesized that KIT is implicated in predisposition to melanoma (MM). Thus, we sequenced the KIT coding region in 112 familial MM cases and 143 matched controls and genotyped tag single‐nucleotide polymorphisms (SNPs) in two cohorts of melanoma patients and matched controls. Five rare KIT substitutions, all predicted possibly or probably deleterious, were identified in five patients, but none in controls [RR = 2.26 (1.26–2.26)]. Expressed in melanocyte lines, three substitutions inhibited KIT signaling. Comparison with exomes database (7020 alleles) confirmed a significant excess of rare deleterious KIT substitutions in patients. Additionally, a common SNP, rs2237028, was associated with MM risk, and 6 KIT variants were associated with nevus count. Our data strongly suggest that rare KIT substitutions predispose to melanoma and that common variants at KIT locus may also impact nevus count and melanoma risk.     

Cesium,Na+-K+ pump and pacemaker potential in cardiac purkinje fibers

The mechanisms of the hyperpolarizing and depolarizing actions of cesium were studied in cardiac Purkinje fibers perfused in vitro by means of a microelectrode technique under conditions that modify either the Na⁺-K⁺ pump activity or I_f. Cs⁺ (2 mM) inconsistently increased and then decreased the maximum diastolic potential (MDP); and markedly decreased diastolic depolarization (DD). Increase and decrease in MDP persisted in fibers driven at fast rate (no diastolic interval and no activation of I_f). In quiescent fibers, Cs⁺ caused a transient hyperpolarization during which elicited action potentials were followed by a markedly decreased undershoot and a much reduced DD. In fibers depolarized at the plateau in zero [K⁺]_o (no I_f), Cs⁺ induced a persistent hyperpolarization. In 2 mM [K⁺]_o, Cs⁺ reduced the undershoot and suppressed spontaneous activity by hyperpolarizing and thus preventing the attainment of the threshold. In 7 mM [K⁺]_o, DD and undershoot were smaller and Cs⁺ reduced them. In 7 and 10 mM [K⁺]_o, Cs⁺ caused a small inconsistent hyperpolarization and a net depolarization in quiescent fibers; and decreased MDP in driven fibers. In the presence of strophanthidin, Cs⁺ hyperpolarized less. Increasing [Cs⁺]_o to 4, 8 and 16 mM gradually hyperpolarized less, depolarized more and abolished the undershoot. We conclude that in Purkinje fibers Cs⁺ hyperpolarizes the membrane by stimulating the activity of the electrogenic Na⁺-K⁺ pump (and not by suppressing I_f); and blocks the pacemaker potential by blocking the undershoot, consistent with a Cs⁺ block of a potassium pacemaker current.     

Comparative selection signature analyses identify genomic footprints in Reggiana cattle,the traditional breed of the Parmigiano-Reggiano cheese production system

Reggiana is an autochthonous cattle breed reared mainly in the province of Reggio Emilia, located in the North of Italy. Reggiana cattle (originally a triple-purpose population largely diffused in the North of Italy) are characterised by a typical solid red coat colour. About 2500 cows of this breed are currently registered to its herd book. Reggiana is now considered a dual-purpose breed even if it is almost completely dedicated to the production of a mono-breed branded Protected Designation of Origin Parmigiano-Reggiano cheese, which is the main driver of the sustainable conservation of this local genetic resource. In this study, we provided the first overview of genomic footprints that characterise Reggiana and define the diversity of this local cattle breed. A total of 168 Reggiana sires (all bulls born over 35 years for which semen was available) and other 3321 sires from 3 cosmopolitan breeds (Brown, Holstein and Simmental) were genotyped with the Illumina BovineSNP50 panel. ADMIXTURE analysis suggested that Reggiana breed might have been influenced, at least in part, by the other three breeds included in this study. Selection signatures in the Reggiana genome were identified using three statistical approaches based on allele frequency differences among populations or on properties of haplotypes segregating in the populations (fixation index (F_ST); integrated haplotype score; cross-population extended haplotype homozygosity). We identified several regions under peculiar selection in the Reggiana breed, particularly on bovine chromosome (BTA) 6 in the KIT gene region, that is known to be involved in coat colour pattern distribution, and within the region of the LAP3, NCAPG and LCORL genes, that are associated with stature, conformation and carcass traits. Another already known region that includes the PLAG1 gene (BTA14), associated with conformation traits, showed a selection signature in the Reggiana cattle. On BTA18, a signal of selection included the MC1R gene that causes the red coat colour in cattle. Other selection sweeps were in regions, with high density of quantitative trait loci for milk production traits (on BTA20) and in several other large regions that might have contributed to shape and define the Reggiana genome (on BTA17 and BTA29). All these results, overall, indicate that the Reggiana genome might still contain several signs of its multipurpose and non-specialised utilisation, as already described for other local cattle populations, in addition to footprints derived by its ancestral origin and by its adaptation to the specialised Parmigiano-Reggiano cheese production system.     

Surface State‐Mediated Charge Transfer of Cs2SnI6 and Its Application in Dye‐Sensitized Solar Cells

A vacancy‐ordered double perovskite, Cs₂SnI₆, has emerged as a promising lead‐free perovskite in the optoelectronic field. However, the charge transfer kinetics mediated by its surface state remains unclear. Here, the charge transfer mechanism of Cs₂SnI₆ is reported and the role of its surface state in the presence of a redox mediator is clarified. Specifically, charge transfer through the surface state of Cs₂SnI₆ and its subsequent surface state charging are demonstrated by cyclic voltammetry and Mott–Schottky measurements, respectively. Because it is expected that the surface state of Cs₂SnI₆ is capable of regenerating oxidized organic dyes, a Cs₂SnI₆‐based regenerator is developed for a dye‐sensitized solar cell composed of fluorine‐doped tin oxide (FTO)/dyed mesoporous TiO₂/regenerator/poly(3,4‐ethylenedioxythiophene)/FTO. As expected, the performance of the Cs₂SnI₆‐based regenerator is strongly dependent on the highest occupied molecular orbital of the dyes. Consequently, Cs₂SnI₆ shows efficient charge transfer with a thermodynamically favorable charge acceptor level, achieving a 79% enhancement in the photocurrent density (14.1 mA cm^?2) compared with that of a conventional liquid electrolyte (7.9 mA cm^?2). The results suggest that the surface state of Cs₂SnI₆ is the main charge transfer pathway in the presence of a redox mediator and should be considered in future designs of Cs₂SnI₆‐based devices.     

Monovalent cation permeabilities of the potassium systems in the crab giant axon

Summary Permeability ratios for pairs of monovalent cations permeating the two potassium systems proposed for the giant axon of the crabCarcinus maenas (M. E. Quinta-Ferreira, E. Rojas & N. Arispe,J. Membrane Biol. 66:171–181, 1982b) were estimated from measurements of the reversal potential of the currents under voltage-clamp conditions. With K⁺ inside the axon, permeability ratios from the reversal potential of the currents through the late channel are:P _Rb/P _K=0.9, /P _K<0.2 andP _Cs/P _K=0.18. With Cs⁺ inside the ratios are:P _K/P _Cs=8.7,P _Rb/P _Cs=7.1 and /P _Cs=2.4. The analysis of the inward currents carried by Rb⁺ or NH ₄ ⁺ showed similar reversal potentials for the early transient component and the late sustained component. Whence, the sequence of permeabilities for the two types of potassium channels is:P _K>P _Rb> >P _Na=P _Cs. The time constants for the activation of the two components recorded either in K-, Rb-, or NH₄-artificial seawater are twice as large as the corresponding time constants measured in Na-artificial seawater.     

Metamorphosis ofHydractinia echinata Insights into pattern formation in Hydroids

Summary Hydractinia echinata is a marine, colony-forming coelenterate. Fertilized eggs develop into freely swimming planula larvae, which undergo metamorphosis to a sessile (primary) polyp. Metamorphosis can be triggered by means of certain marine bacteria and by Cs⁺. Half a day after this treatment a larva will have developed into a polyp. The induction of metamorphosis can be prevented by addition of inhibitor I, a substance partially purified from tissue ofHydra. The larvae ofH. echinata also appear to contain this substance. Inhibitor I appliedafter the onset of metamorphosis blocks its continuation as long as it remains in the culture medium. Cs⁺ applied within the same period of time also blocks the continuation of metamorphosis. However, these two agents have opposite effects on the body pattern of the resultant polyps. The experiments indicate that application of Cs⁺ triggers the generation of the pre-pattern. Inhibitor I appears to be a factor of this prepattern. A model is proposed which describes the basic features of head and foot/stolon formation not only forHydractinia but also for other related hydroids.