<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hisey EA</submitter><funding>University of California Davis Provost Undergraduate Research Fellowship</funding><funding>University of California Davis</funding><funding>University of California Davis Center for Equine Health</funding><funding>University of Califorina Davis Center for Equine Health</funding><funding>National Institutes of Health</funding><funding>National Institute of Food and Agriculture</funding><funding>Morris Animal Foundation</funding><funding>NIH HHS</funding><pagination>848</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7706231</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Distichiasis, an ocular disorder in which aberrant cilia (eyelashes) grow from the opening of the Meibomian glands of the eyelid, has been reported in Friesian horses. These misplaced cilia can cause discomfort, chronic keratitis, and corneal ulceration, potentially impacting vision due to corneal fibrosis, or, if secondary infection occurs, may lead to loss of the eye. Friesian horses represent the vast majority of reported cases of equine distichiasis, and as the breed is known to be affected with inherited monogenic disorders, this condition was hypothesized to be a simply inherited Mendelian trait.&lt;h4>Results&lt;/h4>A genome wide association study (GWAS) was performed using the Axiom 670 k Equine Genotyping array (MNEc670k) utilizing 14 cases and 38 controls phenotyped </pubmed_abstract><journal>BMC genomics</journal><pubmed_title>Whole genome sequencing identified a 16 kilobase deletion on ECA13 associated with distichiasis in Friesian horses.</pubmed_title><pmcid>PMC7706231</pmcid><funding_grant_id>17-24R</funding_grant_id><funding_grant_id>T32 OD010993</funding_grant_id><funding_grant_id>N/A</funding_grant_id><funding_grant_id>16-12</funding_grant_id><funding_grant_id>5T320D010993-12</funding_grant_id><funding_grant_id>2017-67015-26296</funding_grant_id><funding_grant_id>D16EQ-820</funding_grant_id><pubmed_authors>Hisey EA</pubmed_authors><pubmed_authors>Hermans H</pubmed_authors><pubmed_authors>Knickelbein KE</pubmed_authors><pubmed_authors>Avila F</pubmed_authors><pubmed_authors>Lassaline ME</pubmed_authors><pubmed_authors>Duward-Akhurst SA</pubmed_authors><pubmed_authors>Lounsberry ZT</pubmed_authors><pubmed_authors>Grahn RA</pubmed_authors><pubmed_authors>Bellone RR</pubmed_authors><pubmed_authors>Kalbfleisch TS</pubmed_authors><pubmed_authors>Back W</pubmed_authors><pubmed_authors>McCue ME</pubmed_authors></additional><is_claimable>false</is_claimable><name>Whole genome sequencing identified a 16 kilobase deletion on ECA13 associated with distichiasis in Friesian horses.</name><description>&lt;h4>Background&lt;/h4>Distichiasis, an ocular disorder in which aberrant cilia (eyelashes) grow from the opening of the Meibomian glands of the eyelid, has been reported in Friesian horses. These misplaced cilia can cause discomfort, chronic keratitis, and corneal ulceration, potentially impacting vision due to corneal fibrosis, or, if secondary infection occurs, may lead to loss of the eye. Friesian horses represent the vast majority of reported cases of equine distichiasis, and as the breed is known to be affected with inherited monogenic disorders, this condition was hypothesized to be a simply inherited Mendelian trait.&lt;h4>Results&lt;/h4>A genome wide association study (GWAS) was performed using the Axiom 670 k Equine Genotyping array (MNEc670k) utilizing 14 cases and 38 controls phenotyped </description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Nov</publication><modification>2026-05-03T05:00:25.78Z</modification><creation>2021-02-20T03:04:45Z</creation></dates><accession>S-EPMC7706231</accession><cross_references><pubmed>33256610</pubmed><doi>10.1186/s12864-020-07265-8</doi></cross_references></HashMap>