Gabrielle Strobel mentions that DLX5 has been suggested as an MECP2 target. Horike and colleagues report that "transcription of DLX5 and DLX 6 was reproducibly approximately two times higher in Mecp2-null mice" (Holrike et al., 2005). In view of the fact that DLX5 is necessary for osteoblastogenesis and osteoclastogenesis, might we suspect that its increased expression may explain the bone pathology reported in Rett syndrome? Does this resemble Paget disease and if so, might we expect that biphosphonates may be beneficial in Rett syndrome?

References:
Horike S, Cai S, Miyano M, Cheng JF, Kohwi-Shigematsu T. Loss of silent-chromatin looping and impaired imprinting of DLX5 in Rett syndrome. Nat Genet. 2005 Jan;37(1):31-40. Epub 2004 Dec 19. Abstract

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