CFU-Granulocyte (CFU-G), CFU-Macrophage (CFU-M), CFU-Granulocyte/Macrophage (CFU-GM) were identified based on their morphologies (Fig. 4A).
For TL-4, genetic interaction with TL-1 (involving Gm11 and Gm13) permitted identification of the first translocation chromosome (Gm13, and not Gm11); the second (Gm04) was identified through Cent-Gm based FISH karyotyping.
Genetic interaction of TL-5 with TL-2 (Gg01 and Gg08) permitted identification of the first TL-5 translocation chromosome (Gm08, not Gm01); the second (Gm02) was identified through Cent-Gm based FISH karyotyping.
For example, Concibido et al. [ 12] reported the recessive gene rhg 1 that located on Gm 18 was identified to resistant to SCN race 3 and 14 as a major SCN resistance source.
At least one putative W-box was identified in four of the six Gm Hsp20 genes (Gm Hsp22.4, Gm Hsp17.6B, Gm Hsp17.9B and Gm Hsp16.2B) induced by nematodes, but they were all at different positions (−406 bp, -4 bp, -71 bp and −476 bp, respectively).
Exceptions to this pattern were found (Gm Hsp16.2A, Gm Hsp15.2 and Gm Hsp15.4) in which a single putative HSE was identified, occurring approximately 500 bp or more upstream (up to 1,500 bp upstream).
Mammalian Magmas proteins are ubiquitously expressed; and in humans, it was identified as GM-CSF specific signaling molecule which gets overexpressed in neoplastic prostate (41, 42).
More recently, granulocyte-macrophage colony-stimulating factor (GM-CSF) secreted by autoreactive T cells was identified as a potential encephalitogenic factor to sustain neuroinflammation.
Mitemcinal fumarate (6, GM-611), an acid-stable erythromycin derivative with very weak antibiotic activity, was identified as a potent motilin agonist.
Originally, Magmas was identified as a protein involved in granulocyte-macrophage colony-stimulating factor (GM-CSF) signaling and was found to localize in mitochondria.
