{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T00:32:14Z","timestamp":1790641934946,"version":"4.1.0"},"reference-count":61,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,2,16]],"date-time":"2021-02-16T00:00:00Z","timestamp":1613433600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 EY021505"],"award-info":[{"award-number":["R01 EY021505"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["EY029770"],"award-info":[{"award-number":["EY029770"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001209","name":"Knights Templar Eye Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001209","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100002089","name":"Fight for Sight","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100002089","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000001","name":"National Science Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000001","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006094","name":"University of Delaware","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100006094","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"\n Mutations\/deficiency of\n TDRD7<\/jats:italic>\n , encoding a tudor domain protein involved in post-transcriptional gene expression control, causes early onset cataract in humans. While Tdrd7 is implicated in the control of key lens mRNAs, the impact of\n Tdrd7<\/jats:italic>\n deficiency on microRNAs (miRNAs) and how this contributes to transcriptome misexpression and to cataracts, is undefined. We address this critical knowledge-gap by investigating\n Tdrd7<\/jats:italic>\n -targeted knockout (\n Tdrd7-\/-<\/jats:italic>\n ) mice that exhibit fully penetrant juvenile cataracts. We performed Affymetrix miRNA 3.0 microarray analysis on\n Tdrd7-\/-<\/jats:italic>\n mouse lenses at postnatal day (P) 4, a stage preceding cataract formation. This analysis identifies 22 miRNAs [14 over-expressed (miR-15a, miR-19a, miR-138, miR-328, miR-339, miR-345, miR-378b, miR-384, miR-467a, miR-1224, miR-1935, miR-1946a, miR-3102, miR-3107), 8 reduced (let-7b, miR-34c, miR-298, miR-382, miR-409, miR-1198, miR-1947, miR-3092)] to be significantly misexpressed (fold-change \u2265 \u00b1 1.2,\n p<\/jats:italic>\n -value &lt; 0.05) in\n Tdrd7-\/-<\/jats:italic>\n lenses. To understand how these misexpressed miRNAs impact\n Tdrd7-\/-<\/jats:italic>\n cataract, we predicted their mRNA targets and examined their misexpression upon\n Tdrd7<\/jats:italic>\n -deficiency by performing comparative transcriptomics analysis on P4 and P30\n Tdrd7-\/-<\/jats:italic>\n lens. To prioritize these target mRNAs, we used various stringency filters (\n e.g.<\/jats:italic>\n , fold-change in\n Tdrd7-\/-<\/jats:italic>\n lens, iSyTE-based lens-enriched expression) and identified 98 reduced and 89 elevated mRNA targets for overexpressed and reduced miRNAs, respectively, which were classified as \u201ctop-priority\u201d \u201chigh-priority,\u201d and \u201cpromising\u201d candidates. For\n Tdrd7-\/-<\/jats:italic>\n lens overexpressed miRNAs, this approach identified 18 top-priority reduced target mRNAs:\n Alad<\/jats:italic>\n ,\n Ankrd46<\/jats:italic>\n ,\n Ceacam10<\/jats:italic>\n ,\n Dgat2<\/jats:italic>\n ,\n Ednrb<\/jats:italic>\n ,\n H2-Eb1<\/jats:italic>\n ,\n Klhl22<\/jats:italic>\n ,\n Lin7a<\/jats:italic>\n ,\n Loxl1<\/jats:italic>\n ,\n Lpin1<\/jats:italic>\n ,\n Npc1<\/jats:italic>\n ,\n Olfm1<\/jats:italic>\n ,\n Ppm1e<\/jats:italic>\n ,\n Ppp1r1a<\/jats:italic>\n ,\n Rgs8<\/jats:italic>\n ,\n Shisa4<\/jats:italic>\n ,\n Snx22<\/jats:italic>\n and\n Wnk2<\/jats:italic>\n . Majority of these targets were also altered in other gene-specific perturbation mouse models (\n e.g., Brg1<\/jats:italic>\n ,\n E2f1\/E2f2\/E2f3<\/jats:italic>\n ,\n Foxe3<\/jats:italic>\n ,\n Hsf4<\/jats:italic>\n ,\n Klf4<\/jats:italic>\n ,\n Mafg<\/jats:italic>\n \/\n Mafk<\/jats:italic>\n ,\n Notch<\/jats:italic>\n ) of lens defects\/cataract, suggesting their importance to lens biology. Gene ontology (GO) provided further insight into their relevance to lens pathology. For example, the\n Tdrd7<\/jats:italic>\n -deficient lens capsule defect may be explained by reduced mRNA targets (\n e.g., Col4a3<\/jats:italic>\n ,\n Loxl1<\/jats:italic>\n ,\n Timp2<\/jats:italic>\n ,\n Timp3<\/jats:italic>\n ) associated with \u201cbasement membrane\u201d. GO analysis also identified new genes (\n e.g., Casz1<\/jats:italic>\n ,\n Rasgrp1<\/jats:italic>\n ) recently linked to lens biology\/pathology. Together, these analyses define a new Tdrd7-downstream miRNA-mRNA network, in turn, uncovering several new mRNA targets and their associated pathways relevant to lens biology and offering molecular insights into the pathology of congenital cataract.\n <\/jats:p>","DOI":"10.3389\/fcell.2021.615761","type":"journal-article","created":{"date-parts":[[2021,2,18]],"date-time":"2021-02-18T08:49:11Z","timestamp":1613638151000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":20,"title":["Genome-Wide Analysis of Differentially Expressed miRNAs and Their Associated Regulatory Networks in Lenses Deficient for the Congenital Cataract-Linked Tudor Domain Containing Protein TDRD7"],"prefix":"10.3389","volume":"9","author":[{"given":"Deepti","family":"Anand","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Salma","family":"Al Saai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjaya K.","family":"Shrestha","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carrie E.","family":"Barnum","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinichiro","family":"Chuma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Salil A.","family":"Lachke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,2,16]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"717","DOI":"10.1007\/s00439-015-1554-5","article-title":"Compound mouse mutants of bZip transcription factors Mafg and Mafk reveal a regulatory network of non-crystallin genes associated with cataract.","volume":"134","author":"Agrawal","year":"2015","journal-title":"Hum. 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