Project description:We report a mass spectrometry-based proteomics approach to advance the study of the feline proteome. We analyzed immortalized feline cells, various tissues and plasma using data-dependent acquisition (DDA) on a Q Exactive HF mass spectrometer to develop a Felis Catus PeptideAtlas from 157 acquired runs. Data were analyzed using the Trans-Proteomic-Pipeline. We report in the first PeptideAtlas of the domestic cat the identification of 242,844 unique peptides representing 8,972 feline proteins or 45.6% of the predicted UniProtKB Felis catus proteome based on 19,655 unique genes and their representative protein sequences.

2026-07-07 | PXD075481 | Pride

A Mutation in LTBP2 Causes Congenital Glaucoma in Domestic Cats (Felis catus)

Project description:The glaucomas are a group of diseases characterized by optic nerve damage that together represent a leading cause of blindness in the human population and in domestic animals. Here we report a mutation in LTBP2 that causes primary congenital glaucoma (PCG) in domestic cats. We identified a spontaneous form of PCG in cats and established a breeding colony segregating for PCG consistent with fully penetrant, autosomal recessive inheritance of the trait. Elevated intraocular pressure, globe enlargement and elongated ciliary processes were consistently observed in all affected cats by 8 weeks of age. Varying degrees of optic nerve damage resulted by 6 months of age. Although subtle lens zonular instability was a common feature in this cohort, pronounced ectopia lentis was identified in less than 10% of cats examined. Thus, glaucoma in this pedigree is attributed to histologically confirmed arrest in the early post-natal development of the aqueous humor outflow pathways in the anterior segment of the eyes of affected animals. Using a candidate gene approach, significant linage was established on cat chromosome B3 (LOD 18.38, q = 0.00) using tightly linked short tandem repeat (STR) loci to the candidate gene, LTBP2. A 4 base-pair insertion was identified in exon 8 of LTBP2 in affected individuals that generates a frame shift that completely alters the downstream open reading frame and eliminates functional domains. Thus, we describe the first spontaneous and highly penetrant non-rodent model of PCG, identifying a valuable animal model for primary glaucoma that closely resembles the human disease providing valuable insights into mechanisms underlying the disease and a valuable animal model for testing therapies.

2016-05-01 | GSE73263 | GEO

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