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. 2016 May 10;23(5):893–900. doi: 10.1016/j.cmet.2016.04.012

Figure 1.

Figure 1

A 14 bp Deletion in Canine POMC at Position 17: 19431807-19431820 Causes a Frameshift Mutation in the Coding Sequence, Predicted to Stop Production of the Neuroactive Peptide Derivatives β-MSH and β-Endorphin

(A) Chromatogram showing capillary sequencing results from wild-type, homozygous deletion, and heterozygous dogs.

(B) Schematic diagram of POMC showing the pro-peptide and cleavage products. Arrows show di-basic cleavage sites. The mutant peptide is indicated by the position of the red line and results in loss of sequence homology from amino acid 187 of the wild-type dog POMC and a pro-peptide that is 52 amino acids longer. The red box indicates the downstream products that are not produced as a consequence of the mutation.

(C) Alignment of human and canine wild-type POMC and the peptide sequence resulting from the frameshift mutation. Sequence similarity is high (79%) between human and wild-type dog sequences, particularly for cleavage sites (bold type) and neuroactive peptides (highlighted in color). Blue: γ-MSH (human 138–150), ACTH (human 138–176), and α-MSH (human 138–150). Red, peptide products disrupted by mutation: β-MSH (human 217–234) and β-endorphin (human 237–267).