These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Pigment dilution mutants from fish models with connection to lysosome-related organelles and vesicular traffic genes.
    Author: Navarro RE, Ramos-Balderas JL, Guerrero I, Pelcastre V, Maldonado E.
    Journal: Zebrafish; 2008 Dec; 5(4):309-18. PubMed ID: 19133829.
    Abstract:
    An interesting question in developmental biology is why mutations in genes with functions essential for the majority of cells produce diseases affecting only specific tissues. For example, pigment dilution disorders are often the consequence of mutations in conserved vesicular traffic genes. In Hermansky-Pudlak, Griscelli, and Chediak-Higashi pigment dilution syndromes, vesicular traffic mutations affect several organs with one characteristic in common: to carry out their functions they depend to a great extent on lysosome-related organelles (LROs), such as the melanosomes in melanocytes. Conserved multimeric complexes, present in most cell types, target proteins to lysosomes or selected LROs using transport vesicles. By studying these diseases or the model organisms that are defective in these processes, we have learned that every cell type possesses a unique way to regulate its vesicular traffic machinery and to assemble its multimeric complexes. This is accomplished by subunits from these multimeric complexes acting in a cell-specific manner. Here, we review several fish pigment dilution mutants that represent models for human vesicular traffic diseases.
    [Abstract] [Full Text] [Related] [New Search]