The Krüppel-like factor epiprofin is expressed by epithelium of developing teeth, hair follicles, and limb buds and promotes cell proliferation.

We identified a cDNA clone for epiprofin, which is preferentially expressed in teeth, by differential hybridization using DNA microarrays from an embryonic day 19.5 mouse molar cDNA library. Sequence analysis revealed that this cDNA encodes a member of the Krüppel-like factor family containing three characteristic C2H2-type zinc finger motifs. The full-length cDNA was obtained by the 5' Cap capture method. Except for its 5'-terminal sequence, the epiprofin mRNA sequence is almost identical to the predicted sequence of Krüppel-like factor 14/Sp6 (specificity protein 6), which was previously identified in expressed sequence tag data bases and GenBank by an Sp1 zinc finger DNA-binding domain search (Scohy, S., Gabant, P., Van Reeth, T., Hertveldt, V., Dreze, P. L., Van Vooren, P., Riviere, M., Szpirer, J., and Szpirer, C. (2000) Genomics 70, 93-101). This sequence difference is due to differences in the assignment of the location of exon 1. In situ hybridization revealed that epiprofin mRNA is expressed by proliferating dental epithelium, differentiated odontoblast, and also hair follicle matrix epithelium. In addition, whole mount in situ hybridization showed transient expression of epiprofin mRNA in cells of the apical ectodermal ridge in developing limbs and the posterior neuropore. Transfection of an epiprofin expression vector revealed that this molecule is localized in the nucleus and promotes cell proliferation. Thus, epiprofin is a highly cell- and tissue-specific nuclear protein expressed primarily by proliferating epithelial cells of teeth, hair follicles, and limbs that may function in the development of these tissues by regulating cell growth.

Evolutionary adaptation of a mammalian species to an environment severely depleted of iodide.

Lack of dietary iodine is associated with thyroid insufficiency and its dire consequences including cretinism, yet territories severely deficient in iodine are home to many species of wild animals. The premise of our work is that an adaptation must be in place in order to allow these animals to thrive. We collected phyllotine rodents of the genus Auliscomys from the Altiplanic region of North Chile, an area historically associated with goitre and other manifestations of iodine deficiency disorders. The iodide concentration in the stream water in this locality, at <1 micro g l(-1) would undoubtedly result in widespread thyroidal insufficiency in humans and domestic livestock. The animals we collected, identified as Auliscomys boliviensis, showed no evidence of thyroidal insufficiency. There was no enlargement of the thyroid glands; the serum concentrations of thyroid hormone (measured as T4) and thyroid-stimulating hormone were comparable to laboratory rats. Serum iodide concentration was about 40% of that measured in laboratory rats. We conclude that these animals have established a specialised adaptive mechanism, most probably at the level of the Na(+)/I(-) symporter, that acts to enhance the uptake of dietary iodide into the gut and again from the serum into the follicular cells of the thyroid gland.