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J Biol Chem, Vol. 273, Issue 24, 14745-14752, June 12, 1998

The Major Adult -Globin Gene of Antarctic Teleosts and Its Remnants in the Hemoglobinless Icefishes
CALIBRATION OF THE MUTATIONAL CLOCK FOR NUCLEAR GENES

Yuqiong Zhao, Manoja Ratnayake-Lecamwasam, Sandra K. Parker, Ennio Cocca^¶, Laura Camardella^¶, Guido di Prisco^¶, and H. William Detrich III

From the  Department of Biology, Northeastern University, Boston, Massachusetts 02115 and the ^¶ Istituto di Biochimica delle Proteine ed Enzimologia, Consiglio Nazionale delle Ricerche, 80125 Naples, Italy

The icefishes of the Southern Ocean (family Channichthyidae, suborder Notothenioidei) are unique among vertebrates in their inability to synthesize hemoglobin. We have shown previously (Cocca, E., Ratnayake-Lecamwasam, M., Parker, S. K., Camardella, L., Ciaramella, M., di Prisco, G., and Detrich, H. W., III (1995) Proc. Natl. Acad. Sci. U. S. A. 92, 1817-1821) that icefishes retain inactive genomic remnants of adult notothenioid -globin genes but have lost the gene that encodes adult -globin. Here we demonstrate that loss of expression of the major adult -globin, 1, in two species of icefish (Chaenocephalus aceratus and Chionodraco rastrospinosus) results from truncation of the 5' end of the notothenioid 1-globin gene. The wild-type, functional 1-globin gene of the Antarctic yellowbelly rockcod, Notothenia coriiceps, contains three exons and two A + T-rich introns, and its expression may be controlled by two or three distinct promoters. Retained in both icefish genomes are a portion of intron 2, exon 3, and the 3'-untranslated region of the notothenioid 1-globin gene. The residual, nonfunctional -globin gene, no longer under positive selection pressure for expression, has apparently undergone random mutational drift at an estimated rate of 0.12-0.33%/million years. We propose that abrogation of hemoglobin synthesis in icefishes most likely resulted from a single mutational event in the ancestral channichthyid that deleted the entire -globin gene and the 5' end of the linked 1-globin gene.

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