C57BL/6 mice lacking Muc1 show no ocular surface phenotype

PURPOSE. To test the hypothesis that a membrane-spanning mucin, Muc1, facil itates the spread of tear film and protects against bacterial adherence. METHODS. Age-matched, Muc1 null mice and wild-type mice of C57BL/6 genetic background were used for comparison. Eyes were examined by slit lamp biomic roscopy with fluorescein solution to assess epithelial damage and tear him stability. Structure of the ocular surface epithelia was examined by light microscopy, scanning and transmission electron microscopy, and wholemount c onfocal microscopy. Bacterial adherence assay was performed on in vivo corn eas with Pseudomonas aeruginosa containing a plasmid encoding green fluores cent protein, followed by whole-mount confocal microscopy. Real-time revers e transcription-polymerase chain reaction was performed using Muc4-specific primers to quantitate Muc4 mRNA expression in ocular surface tissues. RESULTS. No differences were found between Muc1 null and control mice in an y parameter tested. Ocular surface epithelia of Muc1 null mice of the C57BL /6 strain had a normal appearance of surface microplicae, a well-developed glycocalyx on the apical cell membrane, and a normal appearance of goblet c ell mucin packets. There was no convincing evidence that bacterial adherenc e on the cornea was increased in Muc1 null mice. Muc4 mRNA expression was n ot upregulated in Muc1 null mice compared with control. No ocular surface i nfections were observed in Muc1 null mice of the C57BL/6 strain (n = 204), which were housed in the animal facility over a period of 26 months. CONCLUSIONS. Muc1 null mice of C57BL/6 background appeared normal in all re spects tested. These data differ from the reported phenotype in the mice of the C57BL/6 x SVJ129 background, which show development of blepharitis and conjunctivitis.