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In humans, SIP1 (ZEB2) haploinsufficiency leads to Mowat\u2013Wilson syndrome, a complex congenital anomaly including intellectual disability, epilepsy and Hirschsprung disease. Here we uncover the role of Sip1 in retinogenesis. Somatic deletion of Sip1 from mouse retinal progenitors primarily affects the generation of inner nuclear layer cell types, resulting in complete loss of horizontal cells and reduced numbers of amacrine and bipolar cells, while the number of Muller glia is increased. Molecular analysis places Sip1 downstream of the eye field transcription factor Pax6 and upstream of Ptf1a in the gene network required for generating the horizontal and amacrine lineages. Intriguingly, characterization of differentiation dynamics reveals that Sip1 has a role in promoting the timely differentiation of retinal interneurons, assuring generation of the proper number of the diverse neuronal and glial cell subtypes that constitute the functional retina in mammals.<\/jats:p>","DOI":"10.1242\/dev.136101","type":"journal-article","created":{"date-parts":[[2016,7,7]],"date-time":"2016-07-07T00:48:01Z","timestamp":1467852481000},"page":"2829-2841","source":"Crossref","is-referenced-by-count":12,"title":["Sip1 regulates the generation of the inner nuclear layer retinal cell lineages in mammals"],"prefix":"10.1242","volume":"143","author":[{"given":"Yotam","family":"Menuchin-Lasowski","sequence":"first","affiliation":[{"name":"Sagol School of Neuroscience, Tel-Aviv University 1 Department of Human Molecular Genetics and Biochemistry, Faculty of Medicine and \u2008 , Tel Aviv 69978 , 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