Deformations of Calabi-Yau hypersurfaces arising from deformations of toric varieties

There are easy "polynomial" deformations of Calabi-Yau hypersurfaces in toric varieties performed by changing the coefficients of the defining polynomial of the hypersurface. In this paper, we explicitly constructed the ``non-polynomial'' deformations of Calabi-Yau hypersurfaces, which arise from deformations of the ambient toric variety

Degenerations and mirror contractions of Calabi-Yau complete intersections via Batyrev-Borisov Mirror symmetry

We show that the dual of the Cayley cone, associated to a Minkowski sum decomposition of a reflexive polytope, contains a reflexive polytope admitting a nef-partition. This nef-partition corresponds to a Calabi-Yau complete intersection in a Gorenstein Fano toric variety degenerating to an ample Calabi-Yau hypersurface in another Fano toric variety. Using the Batyrev-Borisov mirror symmetry construction, we found the mirror contraction of a Calabi-Yau complete intersection to the mirror of the ample Calabi-Yau hypersurface

Rpgrip1 is required for rod outer segment development and ciliary protein trafficking in zebrafish

The authors would like to thank the Royal Society of London, the National Eye Research Centre, the Visual Research Trust, Fight for Sight, the W.H. Ross Foundation, the Rosetrees Trust, and the Glasgow Children’s Hospital Charity for supporting this work. This work was also supported by the Deanship of Scientific Research at King Saud University for funding this research (Research Project) grant number ‘RGP – VPP – 219’.Mutations in the RPGR-interacting protein 1 (RPGRIP1) gene cause recessive Leber congenital amaurosis (LCA), juvenile retinitis pigmentosa (RP) and cone-rod dystrophy. RPGRIP1 interacts with other retinal disease-causing proteins and has been proposed to have a role in ciliary protein transport; however, its function remains elusive. Here, we describe a new zebrafish model carrying a nonsense mutation in the rpgrip1 gene. Rpgrip1homozygous mutants do not form rod outer segments and display mislocalization of rhodopsin, suggesting a role for RPGRIP1 in rhodopsin-bearing vesicle trafficking. Furthermore, Rab8, the key regulator of rhodopsin ciliary trafficking, was mislocalized in photoreceptor cells of rpgrip1 mutants. The degeneration of rod cells is early onset, followed by the death of cone cells. These phenotypes are similar to that observed in LCA and juvenile RP patients. Our data indicate RPGRIP1 is necessary for rod outer segment development through regulating ciliary protein trafficking. The rpgrip1 mutant zebrafish may provide a platform for developing therapeutic treatments for RP patients.Publisher PDFPeer reviewe