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PubMed1996

Genetic determination of coat color affects testicular steroidogenesis in the Mustela vison.

Coat color genes in mammals are known to be developmental genes with wide pleiotropic effects. The present study was undertaken to study testicular steroidogenesis in American Mink (Mustela vison) of various coat color phenotypes. No differences in testicular steroid levels were observed between fertile and infertile mink with the standard phenotype and genotype (BB jj MM PP). Mink with the opaline phenotype and genotype (bb mm pp), were found to have in their testes, 20-40% higher levels of progesterone, five times higher levels of 17-hydroxyprogesterone, and eight times higher levels of testosterone, than the corresponding values in other mink. No other differences were observed among the different types of mink. Since the genotype of the opaline mink differs from the other mink studied, only in their combination at the pastel (b) and moyle (m) loci, their bb mm genotype could be assumed to be responsible for the increase in testicular steroids.

17-alpha-Hydroxyprogesterone↗
PubMed1986

Acute and short-term toxicity studies on p-aminodiphenylamine.

p- Aminodiphenylamine (p-ADPA), an aromatic amine of wide industrial applications, also finds human exposure through hair dye preparations or via ingestion of a common food colouring metanil yellow. Acute and short-term toxicity studies in albino rats have been done following the biochemical markers, hematology and tissue histopathology. The acute LD50 value of p-ADPA is 0.847 g/kg body weight which qualifies for the 'moderately toxic' category. In short-term studies, animals were fed p-ADPA, mixed in routine laboratory diet at the concentrations of 0.0 (control), 0.1, 0.25, 0.5 and 0.75% (w/w), daily for 90 days. Feed intake and body weight gain in the highest dosed group were reduced. Hematological examinations exhibited moderate anemic conditions with decreased red blood cells, increased erythrocyte sedimentation rate and lowered packed cell volume suggesting normocytic normochromic anemia at 0.25% onward levels of p-ADPA intake. There was significant increase in the activities of acid/alkaline phosphatases and GOT/GPT in serum with simultaneous depletion from liver at the levels of 0.5 and 0.75% p-ADPA intake, suggesting biochemical lesions of the liver. Testicular LDH and hyaluronidase were lowered at 0.5 and 0.75% levels indicating partial arrest of spermatogenesis. These findings were supported histopathologically. The study warrants careful consideration on its exposure, industrially or through common food color or hair dye preparations.

Anemia↗
PubMed1982

Linkage of the analbuminemia locus (alb) and the hooded locus in the rat, Rattus norvegicus.

A linkage study of the analbuminemia (alb) with some coat color loci (a,b,c,h) has been carried out by crossing the analbuminemic random-bred mutant NAR strain with the abh tester strain of rats, the Agouti-Irish inbred ACI strain and the Agouti-Nonhooded inbred IS strain. The analbuminemia (alb) locus is not linked to a, b, and c loci but linked to hooded locus from F2 and backcross progeny of the F1 hybrids of abh X NAR, ACI X NAR and IS X NAR to NAR. Recombination value between alb and h was 16.4 +/- 2.3 per cent from the data of F2 and backcross progeny of (ACI X NAR) F1 and (IS X NAR) F1 to NAR. This is the third locus on the sixth linkage group of the rat.

Animals↗
PubMed2006

Maternal genistein alters coat color and protects Avy mouse offspring from obesity by modifying the fetal epigenome.

Genistein, the major phytoestrogen in soy, is linked to diminished female reproductive performance and to cancer chemoprevention and decreased adipose deposition. Dietary genistein may also play a role in the decreased incidence of cancer in Asians compared with Westerners, as well as increased cancer incidence in Asians immigrating to the United States. Here, we report that maternal dietary genistein supplementation of mice during gestation, at levels comparable with humans consuming high-soy diets, shifted the coat color of heterozygous viable yellow agouti (A(vy/a) offspring toward pseudoagouti. This marked phenotypic change was significantly associated with increased methylation of six cytosine-guanine sites in a retrotransposon upstream of the transcription start site of the Agouti gene. The extent of this DNA methylation was similar in endodermal, mesodermal, and ectodermal tissues, indicating that genistein acts during early embryonic development. Moreover, this genistein-induced hypermethylation persisted into adulthood, decreasing ectopic Agouti expression and protecting offspring from obesity. Thus, we provide the first evidence that in utero dietary genistein affects gene expression and alters susceptibility to obesity in adulthood by permanently altering the epigenome.

Agouti Signaling Protein↗
PubMed1982

[Coat pigmentation and effect of the ocular retardation gene in the eye of chimeras between or/or and AKR mice].

Twenty-five chimeric adult mice were obtained by aggregating 8-cell embryos of or/or and +/+ genotypes (AKR mice), according to the Tarkovsky and Mints method. The coat color and pigmentary epithelium of the eyes were evidence of chimerism. The coat colour of chimeras varied from a small white to a remarkable gray. The weight of the newborn chimeric mice did not differ from normal. The gene or in homozygotes suppressed the retinal anlage. It was noted that variability of the eye size was dependent on the number of or/or cells in the populations that formed the eyes in chimeras or/or in equilibrium AKR. In 18 animals the eye size did not differ from normal. The pigmentary epithelium of the eyes contained from 32 to 40% or or/or cells. Seven chimeras showed microphthalmos. Asymmetric eye abnormality was recorded in three cases. The pigmentary epithelium of such eyes contained from 63 to 84% or or/or cells.

Animals↗
PubMed1994

Photoperiodic responses in Djungarian hamsters (Phodopus sungorus): importance of light history for pineal and serum melatonin profiles.

Male Djungarian hamsters with previous light experience of long photoperiods of 16 h of light per day (16L:8D) or short photoperiods (8L:16D) were transferred either to the opposite photoperiods or to intermediate photoperiods (14L:10D). It was demonstrated that the same intermediate photoperiod could exert inhibitory or stimulatory effects on coat color, body weight, and the reproductive system, dependent on the previous light history. The response was graduated in accordance with the degree of change in day length. Despite opposite responses to the same photoperiod, diurnal patterns of melatonin in the pineal glands were identical. However, the circadian melatonin pattern in serum of photoinhibited hamsters had a more pronounced nighttime elevation than that found in the serum of photostimulated animals. In hamsters nonresponsive to short photoperiods, no proper short-day pattern was found. Melatonin production is a highly dynamic process, causing concentration shifts in the pineal gland and changes in the serum amplitude during prolonged exposure to short photoperiods. The different reactions to identical photoperiods are associated with different serum melatonin patterns, as shown here for the first time.

Animals↗
PubMed1992

The gene for dominant white color in the pig is closely linked to ALB and PDGRFRA on chromosome 8.

White is a widespread coat color among domestic pig breeds and is controlled by an autosomal dominant gene I. The segregation of this gene was analyzed in a reference pedigree for gene mapping developed by crossing the European wild pig and a Large White domestic breed. The gene for dominant white color was shown to be closely linked to the genes for albumin (ALB) and platelet-derived growth factor receptor alpha (PDGFRA) on chromosome 8. An unexpected phenotype with patches of colored and white coat was observed among the F1 and F2 animals. The segregation data indicated that the phenotype was controlled by a third allele, denoted patch (Ip), most likely transmitted by one of the Large White founder animals. It is shown that the ALB, PDGFRA, I linkage group shares homologies with parts of mouse chromosome 5, human chromosome 4, and horse linkage group II, all of which contain dominant genes for white or white spotting. Candidate genes for the dominant white and patch mutations in the pig are proposed on the basis on these linkage homologies and the recent molecular definition of the dominant white spotting (W) and patch (Ph) mutations in the mouse.

Albumins↗
PubMed1997

Inherited somatic mosaicism caused by an intracisternal A particle insertion in the mouse tyrosinase gene.

A recessive, fully penetrant mutation (c(m1OR)) at the mouse albino locus that results in coat-color mottling has been characterized at the molecular level. Restriction mapping and DNA sequencing analyses provide evidence that mutants carry a 5.4-kb intracisternal A particle (IAP) element insertion upstream of the tyrosinase (Tyr) promoter. Northern blot analysis and reverse transcription-PCR results show that the tyrosinase gene is expressed at much lower levels in mutant than in wild-type mice. The mutant Tyr gene still retains the tissue-specific expression pattern, and the Tyr transcript is not initiated from the IAP long terminal repeat promoter. We propose that the IAP insertion isolates the promoter of the tyrosinase gene from upstream cis-acting regulatory elements, leading to a substantially decreased level of Tyr gene expression in mutants.

Animals↗
PubMed2001

Heritability estimations for diseases, coat color, body weight, and height in a birth cohort of Boxers.

OBJECTIVE: To obtain heritability estimates for diseases and characteristics in Boxers. ANIMALS: Birth cohort of 2,929 purebred Boxers from 414 litters. PROCEDURE: Heritability estimates were determined for cheiloschisis-palatoschisis, cryptorchidism, epilepsy, stifle disorders, cardiac disorders, coat color, birth weight, and adult weight, and height. Binary traits were analyzed by use of a mixed-effects probit model. Some traits also were analyzed by use of a model that postulated monogenic inheritance. Full pedigree analyses were performed. Variation in incidences of disease among clusters of related dogs was evaluated. RESULTS: Heritability estimates were virtually zero for cardiac disorders, medium (0.17 to 0.36) for most other traits, and high (> 0.55) for coat color, birth weight, and adult height. Litter effects and risk factors affected cheiloschisis-palatoschisis, heart murmur, coat color, broadly defined epilepsy, and adult weight. Litter effects may be attributable to common environmental effects for littermates but also may be attributable to dominance variation caused by a recessive gene. Heritability estimates increased when stricter definitions for epilepsy and stifle disorders were used. The monogenic model did not reveal higher heritability estimates for 6 traits analyzed. Incidences for white coat differed significantly for 10 familial clusters, confirming high heritability and effects of familial lineage. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that genetic improvement of most traits should be feasible, except for cardiac disorders. However, because most traits are influenced by environmental effects as well as genetic effects, genetic counseling based on polygenic inheritance and use of familial information rather than strict exclusion of parents is preferred.

Animals↗
PubMed2000

Natural animal coloration can Be determined by a nonfluorescent green fluorescent protein homolog.

It is generally accepted that the colors displayed by living organisms are determined by low molecular weight pigments or chromoproteins that require a prosthetic group. The exception to this rule is green fluorescent protein (GFP) from Aequorea victoria that forms a fluorophore by self-catalyzed protein backbone modification. Here we found a naturally nonfluorescent homolog of GFP to determine strong purple coloration of tentacles in the sea anemone Anemonia sulcata. Under certain conditions, this novel chromoprotein produces a trace amount of red fluorescence (emission lambda(max) = 595 nm). The fluorescence demonstrates unique behavior: its intensity increases in the presence of green light but is inhibited by blue light. The quantum yield of fluorescence can be enhanced dramatically by single amino acid replacement, which probably restores the ancestral fluorescent state of the protein. Other fluorescent variants of the novel protein have emission peaks that are red-shifted up to 610 nm. They demonstrate that long wavelength fluorescence is attainable in GFP-like fluorescent proteins.

Amino Acid Sequence↗
PubMedDate not supplied

Microphthalmia: a morphogenetic lethal mutation of the campbelli hamster (Phodopus campbelli).

Microphthalmia is a new mutation of the campbelli hamster (Phodopus campbelli) that is controlled by an incomplete dominant autosomal gene Mi. The dorsal coat of the heterozygote had dark markings on a white background. The dark markings appear on the head, back, and rump. Their color is very similar to that of the wild type, but slightly lighter. The pupil and iris of the heterozygote are black with reddish tinge. The homozygote has pure white fur all over the body and shows a smaller body size than the wild type and heterozygote. Moreover, the homozygote is characterized by small eyes with unopened eyelids and loss of the incisors. The pupil and iris are colorless and transparent or show a faint reddish tinge when the eyelid is artificially opened. In addition to these abnormalities, individual bones of the homozygote show dwarfism. The parietal and frontal region of the skull are thin and their symphysis is incomplete. The distal regions of the vertebral ribs show swelling. The homozygote is basically lethal within 3 weeks of age. A very few survivors are sterile.

Abnormalities, Multiple↗
PubMed2002

Evidence for translational regulation of the imprinted Snurf-Snrpn locus in mice.

In studies of genomic imprinting in the Prader-Willi/Angelman domain, an agouti coat color cassette was inserted into the downstream open reading frame (ORF) of the imprinted bicistronic Snurf-Snrpn locus in the mouse. The fusion gene was maternally silenced, as is Snurf-Snrpn, and produced a tan abdomen only when inherited paternally in otherwise-black mice. A screen for dominant epigenetic or genetic events was performed with ENU mutagenesis, using a strategy whereby variation in abdominal color was scored at weaning. One mouse with maternal origin of the fusion gene had a tan abdomen and had an imprinting defect resulting in loss of both maternal methylation and silencing of the fusion gene. One mouse with paternal origin of the fusion gene was completely yellow and was found to have an ATG-to-AAG mutation in the initiation codon of the upstream ORF encoding SNURF. Northern blotting, immunoblotting, and transfection studies indicated that the ATG-to-AAG mutation causes a 15-fold or more increase in translation of the downstream ORF in two fusion constructs, and it is likely that similar translational control affects the normal Snurf-Snrpn transcript as well.

Agouti Signaling Protein↗
PubMed1999

Multiple factors in the evolution of animal coloration.

Many of the subjects about which biologists disagree concern the interpretation of function. Morphological, physiological and behavioral characters can simultaneously serve several various functions, all of which are subject to natural selection. These may operate synergistically, but when two produce opposing effects, the one possessing the greater survival value at the time is selected. Often a compromise between several different evolutionary functions results. When the functions under consideration are viewed from a wider angle, a synthesis between differing opinions can sometimes be achieved and a greater understanding of the phenomenon obtained. It should be remembered that, even if an adaptation is invoked for only a brief time during the life of its possessor, it might well be selected merely because of its transient value then. This contribution is not a review, nor is it concerned with the biochemistry and physiology of pigmentation. Rather, it is a discussion of some of the diverse functions that have been ascribed to animal colours. A few typical examples are considered, chosen mainly from among tropical animals including human beings.

Adaptation, Physiological↗
PubMedDate not supplied

Analysis of the inheritance of white spotting and the evaluation of KIT and EDNRB as spotting loci in Dutch boxer dogs.

The genetic basis of the white spotting pattern in Dutch boxer dogs is not known. We studied whether the segregation of white spotting in boxers follows a Mendelian inheritance pattern. Blood samples were collected, along with digital photographs in standard directions of (grand)parents (n=16) and offspring (n=52) from eight litters of Dutch boxers. In order to select heterozygous parents, we selected nonuniform litters, in which at least one puppy was extreme white. On the basis of criteria for the location, the extent of white spotting, and the mean percentage of pigmented area of the foot soles, we classified 10 dogs as solid colored, 27 as flashy, and 15 as extreme white. This was not a significant deviation from the expected 1:2:1 ratio. Because the flashy phenotype seems to be an intermediate between the two homozygotes, white spotting in the Dutch boxer can be considered to be due to a single gene effect, with incomplete dominance. We have evaluated candidate genes c-KIT (KIT) and EDNRB for segregation with white spotting phenotype in these litters. Using polymorphic markers, very near the KIT and EDNRB genes, we found that segregation of the white spotting pattern did not coincide with segregation of these polymorphic markers. Thus neither KIT nor EDNRB are likely to be responsible for white spotting in the Dutch population of boxers.

Animals↗
PubMed1998

A ligand-mimetic model for constitutive activation of the melanocortin-1 receptor.

Dark coat color in the mouse and fox results from constitutively activated melanocortin-1 receptors. Receptor mutations in the mouse (E92K, L98P), cow (L99P), fox (C125R), and sheep (D119N) cluster near the membrane/extracellular junctions of the second and third transmembrane domains, an acidic domain that is the likely site of electrostatic interaction with an arginine residue in the ligand, alpha-MSH. For transmembrane residues E92, D119, and C125, conversion to a basic residue is required for constitutive activation. Unlike constitutively activating mutations in many G protein-coupled receptors that increase agonist efficacy and affinity, these MC1-R mutations have the opposite effect. Therefore, these mutations do not activate the receptor by directly disrupting intramolecular constraints on formation of the active high-affinity state, R*, but do so indirectly by mimicking ligand binding.

Alleles↗
PubMed2004

Dnmt1 expression in pre- and postimplantation embryogenesis and the maintenance of IAP silencing.

The methylation of intracisternal A-type particle (IAP) sequences is maintained during mouse embryogenesis. Methylation suppresses IAP expression and the potential for mutagenesis by retrotransposition, but it is not clear how methylation of these elements is maintained during the embryonic stages when the bulk of the genome is being demethylated. It has been suggested that the high levels of DNA methyltransferase-1 (Dnmt1) present during cleavage could be important for keeping IAPs methylated. To test this hypothesis, we combined mutant alleles of Dnmt1 with an agouti allele (A(iapy)), which provided a coat color readout for the methylation status of the IAP insertion in the agouti locus. We found that reduction in Dnmt1 levels directly impacted methylation at this locus, leading to stable transcriptional activation of the agouti gene in the adult. Specifically, the short maternal Dnmt1 protein was important in maintaining methylation at the A(iapy) locus in cleavage embryos, whereas the longer Dnmt1 isoform found in somatic cells was important in maintaining IAP methylation during the postimplantation stage. These results underscore the importance of maintaining proper maintenance of methylation patterns during gestation and suggest that interference with this process may stably affect gene expression patterns in the adult and may have profound phenotypic consequences.

Agouti Signaling Protein↗
PubMed2004

Giant platelet disorder in the Cavalier King Charles Spaniel.

OBJECTIVE: The aim of this study was to describe the clinical, functional, and morphologic characteristics of platelets in Cavalier King Charles Spaniel dogs (Cavaliers). MATERIALS AND METHODS: Blood from 69 clinically normal Cavaliers was collected and anticoagulated with ethylenediamine-tetraacetic acid (EDTA) and citrate. Automated and manual platelet counts were obtained. Percent platelet aggregation in response to ADP (2, 4, 8, 16, and 32 microM) was determined. Electron microscopy was performed to examine platelet internal morphology and dense granule distribution. A cardiologist recorded the quality of murmurs. RESULTS: Thrombocytopenia (<100,000/microL) was present in 51.43% (36/69) of Cavaliers. Macrothrombocytes (>3 microm) were present in 33.33% (22/69). Mean manual platelet count was 118,770/microL. Manual (EDTA blood) and automated (EDTA and citrated blood) methods of platelet counting were correlated. Prevalence of cardiac murmurs was 38% (26/69). There was no association between affected dogs and murmur, signalment, or coat color. Mean percent platelet aggregation was significantly higher in controls than in Cavaliers (79% vs 38%, p=0.001). Response to ADP was unaffected by thrombocytopenia, macrothrombocytes, murmur, or any combination thereof. Platelet electron microscopy showed normal and giant sized platelets with normal internal morphology. CONCLUSIONS: A benign inherited giant platelet disorder affects approximately 50% of Cavalier King Charles Spaniels. It is characterized by thrombocytopenia, macrothrombocytes, or decreased platelet aggregation in response to ADP. Platelet ultrastructure is normal. Citrated or EDTA blood provides accurate platelet counts. Further studies are indicated to determine platelet glycoprotein structure and any association with mitral endocardiosis. Cavaliers may be useful models of inherited giant platelet disorders.

Adenosine Diphosphate↗
PubMed1994

A molecular model for the genetic and phenotypic characteristics of the mouse lethal yellow (Ay) mutation.

Lethal yellow (Ay) is a mutation at the mouse agouti locus in chromosome 2 that causes a number of dominant pleiotropic effects, including a completely yellow coat color, obesity, an insulin-resistant type II diabetic condition, and an increased propensity to develop a variety of spontaneous and induced tumors. Additionally, homozygosity for Ay results in preimplantation lethality, which terminates development by the blastocyst stage. The Ay mutation is the result of a 170-kb deletion that removes all but the promoter and noncoding first exon of another gene called Raly, which lies in the same transcriptional orientation as agouti and maps 280 kb proximal to the 3' end of the agouti gene. We present a model for the structure of the Ay allele that can explain the dominant pleiotropic effects associated with this mutation, as well as the recessive lethality, which is unrelated to the agouti gene.

Agouti Signaling Protein↗