1 icates that the Clock mutation behaves as an antimorph.

2   Dosage analysis indicates Rld1 mutants are antimorphs.

3                                         Both antimorphs also disrupted the segmental expression of X-

4 s of snr1(E1) reveal that it functions as an antimorph and that snr1 has critical roles in tissue pat

5 rotein is both a mild hypomorph and a potent antimorph as determined by the effect of its expression

6 on profile and displays loss-of-function and antimorph behaviors by impairing and, in some cases, cau

7 t a Vox-activator fusion (VoxG4A) acts as an antimorph, causing the formation of a partial secondary

8 rticle, we show that Sos1 is a semidominant, antimorph mutation.

9 to embryos, and assayed the effects of these antimorphs on somite formation.

10 vation of tumor suppressor genes (hypomorph, antimorph or amorph) or activation of oncogenes (hypermo

11     Most nonsense mutations act as recessive antimorphs, raising the possibility that Fringe may func

12                                   Two of the antimorphs result from identical splice site lesions, wh

13                  In embryos expressing these antimorphs, the paraxial mesoderm differentiated normall