{"id":3965,"date":"2011-02-08T05:00:00","date_gmt":"2011-02-08T10:00:00","guid":{"rendered":"https:\/\/www.med.unc.edu\/biochem\/research-in-yi-zhangs-lab-identifies-a-gene-critical-for-heart-function\/"},"modified":"2018-08-01T10:23:36","modified_gmt":"2018-08-01T14:23:36","slug":"research-in-yi-zhangs-lab-identifies-a-gene-critical-for-heart-function","status":"publish","type":"post","link":"https:\/\/www.med.unc.edu\/biochem\/news\/research-in-yi-zhangs-lab-identifies-a-gene-critical-for-heart-function\/","title":{"rendered":"Research in Yi Zhang’s lab identifies a gene critical for heart function"},"content":{"rendered":"
\n

It\u2019s a gene called DOT1L, and if you don\u2019t have enough of the DOT1L enzyme, you could be at risk for some types of heart disease. These findings by UNC researchers appear in the journal Genes and Development.<\/p>\n

\n
\n \"image2\"\/
Hearts from a wild type control mouse (left) and from a DOT1L-deleted mouse displaying dilated cardiomyopathy (right) . In the absence of DOT1L hearts become severely enlarged, compromising heart function.
\n <\/figcaption><\/figure>\n<\/div>\n
\n

Everyone knows chocolate is critical to a happy Valentine\u2019s Day. Now scientists are one step closer to knowing what makes a heart happy the rest of the year.<\/p>\n

It\u2019s a gene called DOT1L, and if you don\u2019t have enough of the DOT1L enzyme, you could be at risk for some types of heart disease. These findings from a study led by researchers at the University of North Carolina at Chapel Hill School of Medicine appear in the Feb. 1, 2011 issue of the journal Genes and Development.<\/div>\n
The team created a special line of mice that were genetically predisposed to dilated cardiomyopathy, a condition in which the heart expands like a balloon, causing its walls to thin and its pumping ability to weaken. About one in three cases of congestive heart failure is due to dilated cardiomyopathy, a condition that also occurs in children.<\/div>\n
These mice lack DOT1L. The big discovery came when the researchers were able to prevent the mice from developing the disease by re-expressing a single downstream target gene, Dystrophin.<\/div>\n
\u201cWe saw this phenotype in the heart and it could be attributed to anywhere between 1 and 1,000 genes. But when we just added back this one gene, the heart function was completely rescued,\u201d said the study\u2019s lead author, Anh Nguyen, a graduate student in the lab of biochemist Yi Zhang, PhD, at UNC\u2019s Lineberger Comprehensive Cancer Center. \u201cIt was very surprising to us,\u201d Nguyen added. \u201cNormally you\u2019d think you\u2019d have to add in a number of genes to really see that effect.\u201d<\/div>\n
The researchers discovered that the gene depends on the enzyme DOT1L to activate it. If DOT1L levels fall too low, Dystrophin ceases to perform its function, eventually leading to heart disease.<\/div>\n
\u201cWe\u2019ve identified a new function of DOT1L, which has been linked to leukemia before, but never linked to heart defects,\u201d said Zhang, Kenan Distinguished Professor of biochemistry and biophysics and an Investigator of the Howard Hughes Medical Institute.<\/div>\n
Learning how the DOT1L affects Dystrophin could eventually help to improve diagnosis and treatment of patients with dilated cardiomyopathy and other conditions. \u201cThe more we know about the protein, the better we can use it,\u201d Zhang said.<\/div>\n
The protein could be a target for gene therapy, for example. \u201cIf you could manipulate the function of DOT1L, then you could essentially regulate everything else downstream, including Dystrophin or other genes,\u201d explained Nguyen.<\/div>\n
In addition to their experiments using mice, the team examined samples of human heart tissue. Patients with dilated cardiomyopathy had lower levels of DOT1L than patients with no underlying heart condition, suggesting that the protein\u2019s role in humans is similar to its role in mice.<\/div>\n
The findings also have potential relevance for Duchenne muscular dystrophy, which is caused by defects in Dystrophin function. About 90 percent of people with muscular dystrophy develop dilated cardiomyopathy; this study suggests perhaps low levels of DOT1L could be a common factor in both conditions.<\/div>\n
The study\u2019s collaborators include Xiao Xiao, PhD, Fred Eshelman Distinguished Professor of Gene Therapy in the division of molecular pharmaceutics in the UNC School of Pharmacy, Da-Zhi Wang, PhD, of Harvard Medical School, and Taiping Chen, PhD, of Norvartis Institutes for Biomedical Research.<\/div>\n
Media contact: Les Lang, (919) 966-9366, llang@med.unc.edu<\/div>\n

Everyone knows chocolate is critical to a happy Valentine\u2019s Day. Now scientists are one step closer to knowing what makes a heart happy the rest of the year. It\u2019s a gene called DOT1L, and if you don\u2019t have enough of the DOT1L enzyme, you could be at risk for some types of heart disease. These findings from a study led by researchers at the University of North Carolina at Chapel Hill School of Medicine appear in the Feb. 1, 2011 issue of the journal Genes and Development.<\/p>\n

The team created a special line of mice that were genetically predisposed to dilated cardiomyopathy, a condition in which the heart expands like a balloon, causing its walls to thin and its pumping ability to weaken. About one in three cases of congestive heart failure is due to dilated cardiomyopathy, a condition that also occurs in children. These mice lack DOT1L. The big discovery came when the researchers were able to prevent the mice from developing the disease by re-expressing a single downstream target gene, Dystrophin.<\/p>\n

\u201cWe saw this phenotype in the heart and it could be attributed to anywhere between 1 and 1,000 genes. But when we just added back this one gene, the heart function was completely rescued,\u201d said the study\u2019s lead author, Anh Nguyen, a graduate student in the lab of biochemist Yi Zhang, PhD, at UNC\u2019s Lineberger Comprehensive Cancer Center. \u201cIt was very surprising to us,\u201d Nguyen added. \u201cNormally you\u2019d think you\u2019d have to add in a number of genes to really see that effect.\u201d<\/p>\n

The researchers discovered that the gene depends on the enzyme DOT1L to activate it. If DOT1L levels fall too low, Dystrophin ceases to perform its function, eventually leading to heart disease.<\/p>\n

\u201cWe\u2019ve identified a new function of DOT1L, which has been linked to leukemia before, but never linked to heart defects,\u201d said Zhang, Kenan Distinguished Professor of biochemistry and biophysics and an Investigator of the Howard Hughes Medical Institute. Learning how the DOT1L affects Dystrophin could eventually help to improve diagnosis and treatment of patients with dilated cardiomyopathy and other conditions. \u201cThe more we know about the protein, the better we can use it,\u201d Zhang said. The protein could be a target for gene therapy, for example. \u201cIf you could manipulate the function of DOT1L, then you could essentially regulate everything else downstream, including Dystrophin or other genes,\u201d explained Nguyen.<\/p>\n

In addition to their experiments using mice, the team examined samples of human heart tissue. Patients with dilated cardiomyopathy had lower levels of DOT1L than patients with no underlying heart condition, suggesting that the protein\u2019s role in humans is similar to its role in mice.<\/p>\n

The findings also have potential relevance for Duchenne muscular dystrophy, which is caused by defects in Dystrophin function. About 90 percent of people with muscular dystrophy develop dilated cardiomyopathy; this study suggests perhaps low levels of DOT1L could be common factor in both conditions.<\/p>\n

The study\u2019s collaborators include Xiao Xiao, PhD, Fred Eshelman Distinguished Professor of Gene Therapy in the division of molecular pharmaceutics in the UNC School of Pharmacy, Da-Zhi Wang, PhD, of Harvard Medical School, and Taiping Chen, PhD, of Norvartis Institutes for Biomedical Research.<\/p>\n

Media contact: Les Lang, (919) 966-9366, llang@med.unc.edu<\/p>\n<\/div>\n<\/div>\n","protected":false},"excerpt":{"rendered":"

<\/p>\n

It’s a gene called DOT1L, and if you don\u2019t have enough of the DOT1L enzyme, you could be at risk for some types of heart disease. These findings by UNC researchers appear in the journal Genes and Development.<\/p>\n","protected":false},"author":12066,"featured_media":3966,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"layout":"","cellInformation":"","apiCallInformation":"","footnotes":"","_links_to":"","_links_to_target":""},"categories":[2],"tags":[10,16],"class_list":["post-3965","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-news","tag-news_faculty","tag-news_2011","odd"],"acf":[],"yoast_head":"\nResearch in Yi Zhang's lab identifies a gene critical for heart function | Biochemistry and Biophysics<\/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\/biochem\/news\/research-in-yi-zhangs-lab-identifies-a-gene-critical-for-heart-function\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Research in Yi Zhang's lab identifies a gene critical for heart function | Biochemistry and Biophysics\" \/>\n<meta property=\"og:description\" content=\"It's a gene called DOT1L, and if you don\u2019t have enough of the DOT1L enzyme, you could be at risk for some types of heart disease. 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