{"id":3045,"date":"2017-09-21T18:57:51","date_gmt":"2017-09-21T22:57:51","guid":{"rendered":"https:\/\/www.med.unc.edu\/neuroscience\/faulty-cell-signaling-derails-cerebral-cortex-development-could-it-lead-to-autism\/"},"modified":"2018-07-05T13:39:46","modified_gmt":"2018-07-05T17:39:46","slug":"faulty-cell-signaling-derails-cerebral-cortex-development-could-it-lead-to-autism","status":"publish","type":"post","link":"https:\/\/www.med.unc.edu\/neuroscience\/faulty-cell-signaling-derails-cerebral-cortex-development-could-it-lead-to-autism\/","title":{"rendered":"Faulty cell signaling derails cerebral cortex development, could it lead to autism?"},"content":{"rendered":"
\n

<\/p>\n

Anton Lab Researchers pinpoint signaling problems in the progenitor cells crucial for proper neuron generation and organization.<\/p>\n

\n
\"image2\"
Left: typical brain cell organization in control mice. Right: deleting the protein APC in progenitor cells derailed normal neuron generation and migration. (Images: Anton Lab)<\/figcaption><\/figure>\n<\/div>\n
\n

Media contact: Mark Derewicz, 984-974-1915, mark.derewicz@unchealth.unc.edu<\/a><\/p>\n

September 20, 2017<\/p>\n

CHAPEL HILL, NC \u2013 As the embryonic brain develops, an incredibly complex cascade of cellular events occur, starting with progenitors \u2013 the originating cells that generate neurons and spur proper cortex development. If this cascade malfunctions \u2013 if one tiny protein doesn\u2019t do its job \u2013 then the brain could develop abnormally.<\/p>\n

UNC scientists led by Eva Anton, PhD, professor of cell biology and physiology in the UNC School of Medicine, have shown how the deletion of the protein APC in progenitor cells leads to massive disruption of brain development and the canonical Wnt protein pathway \u2013 a signaling cascade\u2013 that previously was linked to genes associated with autism.<\/p>\n

\u201cAlthough our experiments were done in mouse genetic models, human APC mutations have been associated with autism,\u201d said Anton, a member of the UNC Neuroscience Center and the new UNC Autism Research Center. \u201cThese mutations disrupt the ability of brain progenitors to respond appropriately to the environmental cues necessary for them to divide, and to generate and guide neurons during brain development.\u201d<\/p>\n

The Anton lab findings come on the heels of other studies in autism suggesting that, in some cases, the long path toward autism symptoms begins when the development of progenitor cells in the cerebral cortex is disrupted. Other researchers conducted genetic analyses<\/a> of people with autism to discover that the Wnt signaling pathway was disrupted in these patients.<\/p>\n

These two studies led Anton to suspect that something within the Wnt signaling process in progenitor cells could be a culprit, and he set out to test his hypothesis.<\/p>\n

In the developing embryonic brain, Wnt triggers a so-called degradation complex inside the progenitor cell\u2019s cytoplasm. This complex destroys the protein \u03b2-catenin, thus limiting \u03b2-catenin\u2019s ability to enter the nucleus. And that\u2019s important because as progenitor cells divide, this control of b-catenin\u2019s access to the nucleus plays an important role in gene expression and ultimately how neurons are created and how they are channeled to their proper position in various parts of the brain. Given the important role Wnt signaling plays in cell proliferation, it isn\u2019t surprising that Wnt signaling also drives various cancers, as other researchers have found.<\/p>\n

In experiments led by Naoki Nakagawa, PhD, a postdoctoral researcher in Anton\u2019s lab, UNC scientists explored what would happen if they altered the degradation complex. One protein in that complex is APC. When Nakagawa deleted APC, the \u03b2-catenin was left unchecked, triggering unregulated patterns of gene expression in progenitors.<\/p>\n

\u201cIf that happens, everything falls apart,\u201d Anton said. \u201cThe brain doesn\u2019t form properly. We need \u03b2-catenin to get tagged for destruction by that protein complex. If it doesn\u2019t, then Wnt abnormally activates genes in progenitors, causing them to behave abnormally.\u201d<\/p>\n

\"anton<\/p>\n

When Nakagawa titered down \u03b2-catenin in mice that lacked APC, the mice developed normally. In yet another experiment in mice with APC, Anton\u2019s team hyper-activated \u03b2-catenin independent of APC and again the brains didn\u2019t develop properly. \u201cThis showed us that it truly was the deregulation of \u03b2-catenin that caused problems,\u201d Anton said. \u201cAnd it\u2019s APC in that protein complex that\u2019s key to proper regulation.\u201d<\/p>\n

Although this work suggests neuropsychiatric conditions may arise due to mutations in the embryonic brain \u2013 which means it would be much more difficult to medically address \u2013 Anton says it\u2019s too early to say nothing could be done to address problems of Wnt signaling in progenitors, in relation to its role in the rise of autism in children later.<\/p>\n

\u201cWe want to now focus on the syndromic autism genes,\u201d Anton said. \u201cThose are the genes we know<\/i> can cause autism. Some of these genes are expressed in progenitor cells. We want see if deregulation of Wnt signaling triggers changes in syndromic autism gene expression and function in human progenitors,\u201d Anton said.<\/p>\n

For that, Anton\u2019s lab would start with mouse models. If they show that Wnt signaling in progenitors involves autism genes, then Anton\u2019s lab could turn to human progenitor cells and grow them into \u201cminibrains\u201d to study if progenitors are truly affected in autism patients.<\/p>\n

Anton added, \u201cAlthough progenitor defects cannot be treated in mature brain neurons, with such studies we could at least pinpoint what changed and what needs to be corrected in people who develop autism because of subtle but crucial brain changes before birth.\u201d<\/p>\n

The National Institutes of Health funded this research. Other authors included postdoc Keiko Yabuno-Nakagawa, PhD, lab manager Robin Taylor, and former Anton lab postdocs Jingjun Li, PhD, Martin Cowles, PhD, and Tae-Yeon Eom, PhD.<\/i><\/p>\n<\/div>\n<\/div>\n","protected":false},"excerpt":{"rendered":"

<\/p>\n

Anton Lab Researchers pinpoint signaling problems in the progenitor cells crucial for proper neuron generation and organization.<\/p>\n","protected":false},"author":70069,"featured_media":3046,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":"","_links_to":"","_links_to_target":""},"categories":[2],"tags":[4,23,19],"class_list":["post-3045","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-news","tag-4","tag-autism-spectrum-disorder","tag-neurodevelopment","odd"],"acf":[],"yoast_head":"\nFaulty cell signaling derails cerebral cortex development, could it lead to autism? | UNC Neuroscience Center<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.med.unc.edu\/neuroscience\/faulty-cell-signaling-derails-cerebral-cortex-development-could-it-lead-to-autism\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Faulty cell signaling derails cerebral cortex development, could it lead to autism? 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