Function
At the phenomenological level, loss of transmembrane attractin impacts:
Increase in representation of the secreted form is associated with:
- maintenance of myelination - juvenile-onset neuropathology develops
- melanocyte pigmentation - mediates presentation of agouti to Mc1R modifying αMSH signaling to induce pheomelanin production rather than eumelanin
- maintenance of extracellular matrix
- presentation of positively-charged signaling peptides and maintenance of chemokine gradients
Increase in representation of the secreted form is associated with:
- immune cell activation
- inhibition of proper neuronal dendrite development
- developmental progression of gliomas

Expression of surface transmembrane attractin profoundly impacts agouti regulation of pigmentation through Mc1R signaling. As outlined in the panel at left (see credit below), a single amino acid alteration in agouti may affect the presentation mode of agouti to the Mc1R, leading to a reduction in pheomelanin production without a balancing increase in eumelanin production. Conversely, loss of membrane attractin (as observed in the Atrn mutants - see Technical>Research Links tab) leads to a complete block of agouti signaling permitting alpha-MSH-induced eumelanin production.
Graphic by Kellie Holoski/SCIENCE. From F. Pelletier SCIENCE 363:452 (2019) Reprinted with permission from AAAS.
Readers may view, browse, and/or download material for temporary copying purposes only, provided these uses are for noncommercial personal purposes. Except as provided by law, this material may not be further reproduced, distributed, transmitted, modified, adapted, performed, displayed, published, or sold in whole or in part, without prior written permission from the publisher.
Graphic by Kellie Holoski/SCIENCE. From F. Pelletier SCIENCE 363:452 (2019) Reprinted with permission from AAAS.
Readers may view, browse, and/or download material for temporary copying purposes only, provided these uses are for noncommercial personal purposes. Except as provided by law, this material may not be further reproduced, distributed, transmitted, modified, adapted, performed, displayed, published, or sold in whole or in part, without prior written permission from the publisher.