Article

Changes of melanosome morphology associated with the differentiation of epidermal melanocytes in slaty mice

Radiation Effect Mechanism Research Group, National Institute of Radiological Sciences, Anagawa, Inage-ku, Chiba, Japan.
The Anatomical Record Advances in Integrative Anatomy and Evolutionary Biology (Impact Factor: 1.53). 08/2007; 290(8):981-93. DOI: 10.1002/ar.20547
Source: PubMed

ABSTRACT The slaty (Dct(slt)) mutation is known to reduce the activity of dopachrome tautomerase, which converts dopachrome to 5,6-dihydroxyindole-2-carboxylic acid in the pathway of eumelanin synthesis and to inhibit melanosome maturation in melanocytes. However, it is not known whether the inhibition of melanosome maturation in slaty melanocytes is developmentally regulated. To address this point, changes in the morphology and maturation of melanosomes in cultured epidermal melanocytes derived from newborn mice of wild-type (black) and slaty mutant were surveyed under the electron microscope. In black melanocytes (Dct(+)), almost all melanosomes were elliptical stage IV melanosomes. However, in slaty melanocytes, numerous spherical stage III melanosomes with globular depositions of pigment in addition to elliptical stage III melanosomes with intraluminal fibrils were observed. Mixed-type melanosomes containing both globular deposition and intraluminal fibrils of pigment were also observed. In slaty melanocytes, spherical and mixed-type melanosomes were gradually decreased after birth, whereas elliptical melanosomes were gradually increased. Stage IV melanosomes were very few in slaty melanocytes, and the number did not increase after birth. These results suggest that the slaty mutation blocks the melanosome maturation at stage III and affects the melanosome morphology (elliptical or spherical) in a developmental stage-specific manner.

Download full-text

Full-text

Available from: Tomohisa Hirobe, Apr 04, 2014
0 Followers
 · 
73 Views
 · 
23 Downloads
  • Source
    • "It has been reported that the slaty (Dct slt /Dct slt , with a reduced Tyrp2 activity) melanocytes possess ellipsoidal melanosomes, round melanosomes with granular depositions and mixed type of both melanosomes in a ratio of 4.5:4.5:1, and possess a large number of immature stage III melanosomes (Hirobe and Abe, 2007). These results suggest that the formation of ellipsoidal melanosomes is inhibited by reducing the activity of Tyrp1 or Tyrp2. "
    [Show abstract] [Hide abstract]
    ABSTRACT: B (Tyrp1 (+)), the wild type allele at the mouse brown locus, produces black eumelanin, while b (Tyrp1(b) ), the recessive allele, produces brown eumelanin and exhibits lower tyrosinase (Tyr)-related protein 1 (Tyrp1) activity. However, it is unknown whether melanocyte proliferation and differentiation are affected by the Tyrp1(b) mutation. The proliferation rate of brown (C57BL/10JHir (B10)-Tyrp1(b) / Tyrp1(b) ) melanocytes cultured in a serum-free melanocyte proliferation medium (MDMD) was similar to that of black (B10-Tyrp1(+)/Tyrp1(+) ) melanocytes. Although brown melanocytes exhibited normal morphology, their pigmentation was lower than that of black melanocytes. However, Tyr activity in brown melanocytes was increased both in vivo and in vitro. Melanosomes of cultured brown melanocytes were mostly spherical stage III melanosomes with granular depositions of pigments, whereas those of cultured black melanocytes were mostly stage IV ellipsoidal melanosomes with pigment depositions in intraluminal fibrils. Chemical analysis of melanin present in dorsal hairs of 5-week-old mice from the F2 generation between brown and recessive yellow (B10-Mc1r(e)/Mc1r(e) ) or agouti (B10-A/A) mice showed that eumelanin content was greatly decreased in brown and brown agouti (cinnamon) mice, whereas pheomelanin contents in brown recessive yellow and cinnamon mice did not differ from the corresponding Tyrp1(+)/- mice. These results suggest that the brown allele greatly inhibits eumelanin, but not pheomelanin synthesis.
    ZOOLOGICAL SCIENCE 02/2014; 31(2):53-63. DOI:10.2108/zsj.31.53 · 0.88 Impact Factor
  • Source
    • "(Anderson et al., 2008). The production of brown-black pigment or eumelanin is a multistep chemical reaction regulated by multiple gene products including Tyrp1 (tyrosinase-related protein 1) and Dct (dopachrome delta-isomerase, tyrosine-related protein 2) (Hirobe and Abe, 2007; Matsunaga et al., 2002; Solano et al., 2000; Winder et al., 1994). Gene products such as Oca2 (oculocutaneous albinism II) and Myo5a (myosin VA) have also been found to be critical for melanogenesis. "
    08/2013; DOI:10.14304/SURYA.JPR.V1N8.8
  • Source
    • "(Anderson et al., 2008). The production of brown-black pigment or eumelanin is a multistep chemical reaction regulated by multiple gene products including Tyrp1 (tyrosinase-related protein 1) and Dct (dopachrome delta-isomerase, tyrosine-related protein 2) (Hirobe and Abe, 2007; Matsunaga et al., 2002; Solano et al., 2000; Winder et al., 1994). Gene products such as Oca2 (oculocutaneous albinism II) and Myo5a (myosin VA) have also been found to be critical for melanogenesis. "
    [Show abstract] [Hide abstract]
    ABSTRACT: We investigated the contributions of Tyrp1 and Gpnmb to the iris transillumination defect (TID) in five age cohorts of BXD mice. Using systems genetics, we also evaluated the role of other known pigmentation genes (PGs). Mapping studies indicate that Tyrp1 contributes to the phenotype at all ages, yet the TID maps to Gpnmb only in the oldest cohort. Composite interval mapping reveals secondary loci viz. Oca2, Myo5a, Prkcz and Zbtb20 that modulate the phenotype in the age groups up to 10-13 months. The contributions of Tyrp1 and Gpnmb were highly significant in all age cohorts. Moreover, in young mice, all six gene candidates had substantial interactions in our model. Our model accounted for 71-88% of the explained variance of the TID phenotype across the age bins. These results demonstrate that along with Tyrp1 and Gpnmb, Oca2, Myo5a, Prkcz and Zbtb20 modulate the TID in an age-dependent manner. This article is protected by copyright. All rights reserved.
    Pigment Cell & Melanoma Research 04/2013; 26(4). DOI:10.1111/pcmr.12106 · 5.64 Impact Factor
Show more