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Melanosome‐autonomous regulation of size and number: the OA 1 receptor sustains PMEL expression
Author(s) -
Falletta Paola,
Bagnato Paola,
Bono Maria,
Monticone Massimiliano,
Schiaffino Maria Vittoria,
Bennett Dorothy C.,
Goding Colin R.,
Tacchetti Carlo,
Valetti Caterina
Publication year - 2014
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/pcmr.12239
Subject(s) - melanosome , microbiology and biotechnology , receptor , biology , genetics , melanin
Summary Little is known as to how cells ensure that organelle size and number are coordinated to correctly couple organelle biogenesis to the demands of proliferation or differentiation. OA 1 is a melanosome‐associated G ‐protein‐coupled receptor involved in melanosome biogenesis during melanocyte differentiation. Cells lacking OA 1 contain fewer, but larger, mature melanosomes. Here, we show that OA 1 loss of function reduces both the basal expression and the α‐melanocyte‐stimulating hormone/c AMP ‐dependent induction of the microphthalmia‐associated transcription factor ( MITF ), the master regulator of melanocyte differentiation. In turn, this leads to a significant reduction in expression of PMEL , a major melanosomal structural protein, but does not affect tyrosinase and melanin levels. In line with its pivotal role in sensing melanosome maturation, OA 1 expression rescues melanosome biogenesis, activates MITF expression and thereby coordinates melanosome size and number, providing a quality control mechanism for the organelle in which resides. Thus, resident sensor receptors can activate a transcriptional cascade to specifically promote organelle biogenesis.