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Although originally named because of their ability to induce bone and cartilage formation [ 15 ] , BMPs are involved in many developmental processes, including cell proliferation and differentiation, apoptosis, and intercellular interactions during morphogenesis [ 16 17 18 19 20 21 22 23 24 25 ] . Members of the bone morphogenetic protein family function in a gene dosage dependent manner during development and participate in ocular development [ 26 27 28 29 ] . Therefore, mutations that alter the level of BMPs or alter the degree of BMP signaling are candidates to contribute to Axenfeld-Rieger syndrome and other conditions involving anterior segment malformation, elevated IOP, and glaucoma.
Interestingly, some BMPs modulate tooth morphogenesis [ 30 ] and Axenfeld-Rieger patients present with dental abnormalities.
Glaucoma is a leading cause of blindness that involves loss of retinal ganglion cells and degeneration of the optic nerve [ 1 ] . Glaucoma is usually associated with high intraocular pressure (IOP) that results from an increased resistance to drainage of the ocular fluid [ 1 ] . Developmental disorders of the ocular anterior segment, including Axenfeld-Rieger syndrome, are often associated with elevated IOP and glaucoma [ 1 2 ] . The developmental sequence and structure of the human and mouse ocular drainage structures are similar [ 3 ] , and the same genes are known to cause anterior segment dysgenesis (ASD) in humans and mice.
The ocular phenotypes of Bmp4 mutant mice show that BMP4 is a strong candidate to contribute to Axenfeld-Rieger anomaly and other developmental conditions associated with human glaucoma.
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