Fig. 4

Sequence analysis of Crystallin variants: a CRYAA –wild type and missense variant c.145C>T in unaffected and affected member of family—A with nuclear cataract; b CRYBA1—an indel variant at c.272delG in an affected member of family B with nuclear cataract; c CRYGD—wild type in unaffected and stop codon variant c.470G>A in affected member of family—C with pulverulent cataract; d CRYGC—a frameshift mutation at c.179delG is shown in the affected member of family-D with nuclear cataract; e CRYBB1—a stop codon variant c.656G>A in an affected member of family-E with lamellar cataract; f CRYGD– mutant stop codon amino acid at c.392G>A in an affected female with nuclear cataract; g CRYAA—a mutant indel variant at c.454delG in affected male with congenital cataract and (G1) CRYGA—another missense novel disease-causing variant of uncertain significance at c.118A>T in the same individual G; h CRYBB1—a stop codon mutation at c.618C>A in affected female with congenital cataract; i CRYGC—a missense variant at c.13A>C in an affected male with congenital cataract and j CRYGD a stop codon variant at c.418C>T in an affected female with nuclear cataract