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Article: MYT1L deficiency impairs excitatory neuron trajectory during cortical development.

Yen, Allen / Chen, Xuhua / Skinner, Dominic D / Leti, Fatjon / Crosby, MariaLynn / Hoisington-Lopez, Jessica / Wu, Yizhe / Chen, Jiayang / Mitra, Robi D / Dougherty, Joseph D

bioRxiv : the preprint server for biology

2024

Abstract: Mutations that reduce the function of MYT1L, a neuron-specific transcription factor, are associated with a syndromic neurodevelopmental disorder. Furthermore, MYT1L is routinely used as a proneural factor in fibroblast-to-neuron transdifferentiation. ... ...

Abstract	Mutations that reduce the function of MYT1L, a neuron-specific transcription factor, are associated with a syndromic neurodevelopmental disorder. Furthermore, MYT1L is routinely used as a proneural factor in fibroblast-to-neuron transdifferentiation. MYT1L has been hypothesized to play a role in the trajectory of neuronal specification and subtype specific maturation, but this hypothesis has not been directly tested, nor is it clear which neuron types are most impacted by MYT1L loss. In this study, we profiled 313,335 nuclei from the forebrains of wild-type and MYT1L-deficient mice at two developmental stages: E14 at the peak of neurogenesis and P21, when neurogenesis is complete, to examine the role of MYT1L levels in the trajectory of neuronal development. We found that MYT1L deficiency significantly disrupted the relative proportion of cortical excitatory neurons at E14 and P21. Significant changes in gene expression were largely concentrated in excitatory neurons, suggesting that transcriptional effects of MYT1L deficiency are largely due to disruption of neuronal maturation programs. Most effects on gene expression were cell autonomous and persistent through development. In addition, while MYT1L can both activate and repress gene expression, the repressive effects were most sensitive to haploinsufficiency, and thus more likely mediate MYT1L syndrome. These findings illuminate the intricate role of MYT1L in orchestrating gene expression dynamics during neuronal development, providing insights into the molecular underpinnings of MYT1L syndrome.
Language	English
Publishing date	2024-03-07
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.06.583632
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Article ; Online: Development of Targeted Therapies Based on Gene Modification.

Benson, Taylor M / Leti, Fatjon / DiStefano, Johanna K

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1706, Page(s) 39–51

Abstract: With the advent of next-generation sequencing (NGS) and the demand for a personalized healthcare system, the fields of precision medicine and gene therapy are advancing in new directions. There is a push to identify genes that contribute to disease ... ...

Abstract	With the advent of next-generation sequencing (NGS) and the demand for a personalized healthcare system, the fields of precision medicine and gene therapy are advancing in new directions. There is a push to identify genes that contribute to disease development, either alone or in conjunction with other genes or environmental factors, and then design targeted therapies based on this knowledge, rather than the traditional approach of treating generalized symptoms with pharmaceuticals in a one-size-fits-all manner. Identification of genes that contribute to disease pathogenesis and progression is critical for the maturation of the precision medicine field. Concomitant with a better understanding of disease pathology, precision medicine approaches can be adopted with greater confidence and are expected to lead to a new standard for clinical practice. In this chapter, we provide a brief introduction to precision medicine, discuss the importance of identifying genes and genetic variants that contribute to disease development and progression, offer examples of approaches that can be applied to treat specific diseases, and present some of the current challenges and limitations of precision medicine.
MeSH term(s)	Animals ; Gene-Environment Interaction ; Genetic Therapy/methods ; Genetic Variation ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Precision Medicine/methods
Language	English
Publishing date	2018-01-21
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-7471-9_3
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Article ; Online: miRNA Quantification Method Using Quantitative Polymerase Chain Reaction in Conjunction with C

Leti, Fatjon / DiStefano, Johanna K

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1706, Page(s) 257–265

Abstract: MicroRNAs are small noncoding RNAs that function to regulate gene expression. In general, miRNAs are posttranscriptional regulators that imperfectly bind to the 3'untranslated region (3'UTR) of target mRNAs bearing complementary sequences, and target ... ...

Abstract	MicroRNAs are small noncoding RNAs that function to regulate gene expression. In general, miRNAs are posttranscriptional regulators that imperfectly bind to the 3'untranslated region (3'UTR) of target mRNAs bearing complementary sequences, and target more than half of all protein-coding genes in the human genome. The dysregulation of miRNA expression and activity has been linked with numerous diseases, including cancer, cardiovascular diseases, neurodegenerative disorders, and diabetes. To better understand the relationship between miRNAs and human disease, a variety of techniques have been used to measure and validate miRNA expression in many cells, tissues, body fluids, and organs. For many years, quantitative polymerase chain reaction (qPCR) has been the gold standard for measuring relative gene expression, and is now also widely used to assess miRNA abundance. In this chapter, we describe a quick protocol for miRNA extraction, reverse transcription, qPCR, and data analysis.
MeSH term(s)	Animals ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Diabetes Mellitus/genetics ; Diabetes Mellitus/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs/biosynthesis ; MicroRNAs/genetics ; Neoplasms/genetics ; Neoplasms/metabolism ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; RNA, Neoplasm/biosynthesis ; RNA, Neoplasm/genetics ; Real-Time Polymerase Chain Reaction/methods
Chemical Substances	MicroRNAs ; RNA, Neoplasm
Language	English
Publishing date	2018-02-08
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-7471-9_14
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Article: Long Noncoding RNAs as Diagnostic and Therapeutic Targets in Type 2 Diabetes and Related Complications.

Leti, Fatjon / DiStefano, Johanna K

Genes

2017 Volume 8, Issue 8

Abstract: Protein-coding genes represent only a small fraction of the human genome. In the past, the majority of the genomic sequence has been considered transcriptionally silent, but recent large-scale studies have uncovered an array of functionally significant ... ...

Abstract	Protein-coding genes represent only a small fraction of the human genome. In the past, the majority of the genomic sequence has been considered transcriptionally silent, but recent large-scale studies have uncovered an array of functionally significant elements, including non-protein-coding transcripts, within these noncoding regions of the human genome. Long noncoding RNAs (lncRNAs), a class of noncoding transcripts with lengths >200 nucleotides, are pervasively transcribed in the genome and function as signals, decoys, guides, or scaffolds to regulate gene expression. More than 200 diseases have been associated with dysregulated or dysfunctional lncRNAs, and new associations continue to accumulate in the literature. The role of lncRNAs in the pathogenesis of type 2 diabetes mellitus and related complications has only recently been recognized, but there is already evidence for their involvement in many of the pathophysiological mechanisms underlying the disease. In this review, we summarize the current knowledge of the functions and underlying mechanisms of lncRNA activity with a focus on type 2 diabetes mellitus and related renal and retinal complications of the disease. We also discuss the potential of lncRNAs to serve as therapeutic targets for drug development and diagnostic markers for clinical applications in the management of diabetes.
Language	English
Publishing date	2017-08-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes8080207
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Article: Long noncoding RNAs in the pathogenesis of diabetic kidney disease: implications for novel therapeutic strategies.

Leti, Fatjon / Morrison, Evan / DiStefano, Johanna K

Personalized medicine

2017 Volume 14, Issue 3, Page(s) 271–278

Abstract: Diabetic kidney disease is a progressive disorder that develops secondary to diabetes. Current strategies for the clinical management of the disease can delay its onset and prevent progression, yet a significant proportion of patients still develop renal ...

Abstract	Diabetic kidney disease is a progressive disorder that develops secondary to diabetes. Current strategies for the clinical management of the disease can delay its onset and prevent progression, yet a significant proportion of patients still develop renal failure. The need for more advanced pharmaceuticals is therefore critical for improved treatment strategies. Recent studies support a role for long noncoding RNAs (lncRNAs) in the pathogenesis of human disease. Here we review recent experimental results linking lncRNAs with diabetic kidney disease. A better understanding of the regulatory role that lncRNAs play in the development of diabetic kidney disease may lead to identification of novel targets for therapeutic intervention.
MeSH term(s)	Diabetes Complications ; Diabetic Nephropathies/genetics ; Diabetic Nephropathies/pathology ; Disease Progression ; Gene Expression Regulation/genetics ; Humans ; Kidney/pathology ; Precision Medicine ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
Chemical Substances	RNA, Long Noncoding
Language	English
Publishing date	2017-05-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2299146-3
ISSN	1744-828X ; 1741-0541
ISSN (online)	1744-828X
ISSN	1741-0541
DOI	10.2217/pme-2016-0107
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Article ; Online: Methods for CpG Methylation Array Profiling Via Bisulfite Conversion.

Leti, Fatjon / Llaci, Lorida / Malenica, Ivana / DiStefano, Johanna K

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1706, Page(s) 233–254

Abstract: DNA methylation is a key factor in epigenetic regulation, and contributes to the pathogenesis of many diseases, including various forms of cancers, and epigenetic events such X inactivation, cellular differentiation and proliferation, and embryonic ... ...

Abstract	DNA methylation is a key factor in epigenetic regulation, and contributes to the pathogenesis of many diseases, including various forms of cancers, and epigenetic events such X inactivation, cellular differentiation and proliferation, and embryonic development. The most conserved epigenetic modification in plants, animals, and fungi is 5-methylcytosine (5mC), which has been well characterized across a diverse range of species. Many technologies have been developed to measure modifications in methylation with respect to biological processes, and the most common method, long considered a gold standard for identifying regions of methylation, is bisulfite conversion. In this technique, DNA is treated with bisulfite, which converts cytosine residues to uracil, but does not affect cytosine residues that have been methylated, such as 5-methylcytosines. Following bisulfite conversion, the only cytosine residues remaining in the DNA, therefore, are those that have been methylated. Subsequent sequencing can then distinguish between unmethylated cytosines, which are displayed as thymines in the resulting amplified sequence of the sense strand, and 5-methylcytosines, which are displayed as cytosines in the resulting amplified sequence of the sense strand, at the single nucleotide level. In this chapter, we describe an array-based protocol for identifying methylated DNA regions. We discuss protocols for DNA quantification, bisulfite conversion, library preparation, and chip assembly, and present an overview of current methods for the analysis of methylation data.
MeSH term(s)	5-Methylcytosine/chemistry ; Animals ; CpG Islands ; DNA Methylation ; Humans ; Oligonucleotide Array Sequence Analysis/instrumentation ; Oligonucleotide Array Sequence Analysis/methods ; Sequence Analysis, DNA/instrumentation ; Sequence Analysis, DNA/methods ; Sulfites/chemistry
Chemical Substances	Sulfites ; 5-Methylcytosine (6R795CQT4H) ; hydrogen sulfite (OJ9787WBLU)
Language	English
Publishing date	2018-02-08
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-7471-9_13
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Article ; Online: Altered expression of MALAT1 lncRNA in nonalcoholic steatohepatitis fibrosis regulates CXCL5 in hepatic stellate cells.

Leti, Fatjon / Legendre, Christophe / Still, Christopher D / Chu, Xin / Petrick, Anthony / Gerhard, Glenn S / DiStefano, Johanna K

Translational research : the journal of laboratory and clinical medicine

2017 Volume 190, Page(s) 25–39.e21

Abstract: In the present study, we sought to identify long noncoding RNA (lncRNA) expression profiles in nonalcoholic steatohepatitis (NASH) patients with histologic evidence of lobular inflammation and advanced fibrosis. We profiled lncRNA expression using RNA- ... ...

Abstract	In the present study, we sought to identify long noncoding RNA (lncRNA) expression profiles in nonalcoholic steatohepatitis (NASH) patients with histologic evidence of lobular inflammation and advanced fibrosis. We profiled lncRNA expression using RNA-sequencing of wedge liver biopsies from 24 nonalcoholic fatty liver disease (NAFLD) patients with normal liver histology, 53 NAFLD patients with lobular inflammation, and 65 NAFLD patients with advanced fibrosis. Transcript profiling identified 4432 and 4057 differentially expressed lncRNAs in comparisons of normal tissue with lobular inflammation and fibrosis samples, respectively. Functional enrichment analysis revealed lncRNA participation in transforming growth factor beta 1 and tumor necrosis factor signaling, insulin resistance, and extracellular matrix maintenance. Several lncRNAs were highly expressed in fibrosis relative to normal tissue, including nuclear paraspeckle assembly transcript 1, hepatocellular carcinoma upregulated lncRNA, and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). Two potential target mRNAs, syndecan 4 (SDC4), and C-X-C motif chemokine ligand 5 (CXCL5) were identified for hepatocellular carcinoma upregulated lncRNA and MALAT1, respectively, but only CXCL5 showed differential expression among the different histologic classes. Knockdown of MALAT1 expression reduced CXCL5 transcript and protein levels by 50% and 30%, respectively, in HepG2 cells. The expression of MALAT1 and CXCL5 was upregulated in activated hepatic stellate (LX-2) cells compared to cells in the quiescent state, and MALAT1 expression was regulated by hyperglycemia and insulin in HepG2 cells, but only by insulin in LX-2 cells. Dysregulated lncRNA expression is associated with inflammation and fibrosis in NASH. Functionally relevant differences in MALAT1 expression may contribute to the development of fibrosis in NASH through mechanisms involving inflammatory chemokines.
MeSH term(s)	Chemokine CXCL5/genetics ; Chemokine CXCL5/metabolism ; Hepatic Stellate Cells/metabolism ; Humans ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Metabolic Networks and Pathways ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/pathology ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Transcriptome
Chemical Substances	CXCL5 protein, human ; Chemokine CXCL5 ; MALAT1 long non-coding RNA, human ; RNA, Long Noncoding
Language	English
Publishing date	2017-09-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2246684-8
ISSN	1878-1810 ; 1532-6543 ; 1931-5244
ISSN (online)	1878-1810 ; 1532-6543
ISSN	1931-5244
DOI	10.1016/j.trsl.2017.09.001
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Article ; Online: The Arg59Trp variant in ANGPTL8 (betatrophin) is associated with total and HDL-cholesterol in American Indians and Mexican Americans and differentially affects cleavage of ANGPTL3.

Hanson, Robert L / Leti, Fatjon / Tsinajinnie, Darwin / Kobes, Sayuko / Puppala, Sobha / Curran, Joanne E / Almasy, Laura / Lehman, Donna M / Blangero, John / Duggirala, Ravindranath / DiStefano, Johanna K

Molecular genetics and metabolism

2016 Volume 118, Issue 2, Page(s) 128–137

Abstract: We previously identified a locus linked to total cholesterol (TC) concentration in Pima Indians on chromosome 19p. To characterize this locus, we genotyped >2000 SNPs in 1838 Pimas and assessed association with log(TC). We observed evidence for ... ...

Abstract	We previously identified a locus linked to total cholesterol (TC) concentration in Pima Indians on chromosome 19p. To characterize this locus, we genotyped >2000 SNPs in 1838 Pimas and assessed association with log(TC). We observed evidence for association with log(TC) with rs2278426 (3.5% decrease/copy of the T allele; P=5.045×10(-6)) in the ANGPTL8 (angiopoietin-like 8) gene. We replicated this association in 2413 participants of the San Antonio Mexican American Family Study (SAMAFS: 2.0% decrease per copy of the T allele; P=0.005842). In a meta-analysis of the combined data, we found the strongest estimated effect with rs2278426 (P=2.563×10(-7)). The variant T allele at rs2278426 predicts an Arg59Trp substitution and has previously been associated with LDL-C and HDL-C. In Pimas and SAMAFS participants, the T allele of rs2278426 was associated with reduced HDL-C levels (P=0.000741 and 0.00002, respectively), and the combined estimated effect for the two cohorts was -3.8% (P=8.526×10(-8)). ANGPTL8 transcript and protein levels increased in response to both glucose and insulin. The variant allele was associated with increased levels of cleaved ANGPTL3. We conclude that individuals with the variant allele may have lower TC and HDL-C levels due to increased activation of ANGPTL3 by ANGPTL8.
Language	English
Publishing date	2016-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	1418518-0
ISSN	1096-7206 ; 1096-7192
ISSN (online)	1096-7206
ISSN	1096-7192
DOI	10.1016/j.ymgme.2016.04.007
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Article ; Online: High-throughput sequencing reveals altered expression of hepatic microRNAs in nonalcoholic fatty liver disease-related fibrosis.

Leti, Fatjon / Malenica, Ivana / Doshi, Meera / Courtright, Amanda / Van Keuren-Jensen, Kendall / Legendre, Christophe / Still, Christopher D / Gerhard, Glenn S / DiStefano, Johanna K

Translational research : the journal of laboratory and clinical medicine

2015 Volume 166, Issue 3, Page(s) 304–314

Abstract: Recent evidence suggests that microRNAs (miRNAs), small, noncoding RNA molecules that regulate gene expression, may play a role in the regulation of metabolic disorders, including nonalcoholic fatty liver disease (NAFLD). To identify miRNAs that mediate ... ...

Abstract	Recent evidence suggests that microRNAs (miRNAs), small, noncoding RNA molecules that regulate gene expression, may play a role in the regulation of metabolic disorders, including nonalcoholic fatty liver disease (NAFLD). To identify miRNAs that mediate NAFLD-related fibrosis, we used high-throughput sequencing to assess miRNAs obtained from liver biopsies of 15 individuals without NAFLD fibrosis (F0) and 15 individuals with severe NAFLD fibrosis or cirrhosis (F3-F4), matched for age, sex, body mass index, type 2 diabetes status, hemoglobin A1c, and use of diabetes medications. We used DESeq2 and Kruskal-Wallis test to identify miRNAs that were differentially expressed between NAFLD patients with or without fibrosis, adjusting for multiple testing using Bonferroni correction. We identified a total of 75 miRNAs showing statistically significant evidence (adjusted P value <0.05) for differential expression between the 2 groups, including 30 upregulated and 45 downregulated miRNAs. Quantitative reverse-transcription polymerase chain reaction analysis of selected miRNAs identified by sequencing validated 9 of 11 of the top differentially expressed miRNAs. We performed functional enrichment analysis of dysregulated miRNAs and identified several potential gene targets related to NAFLD-related fibrosis including hepatic fibrosis, hepatic stellate cell activation, transforming growth factor beta signaling, and apoptosis signaling. We identified forkhead box O3 and F-box WD repeat domain containing 7, E3 ubiquitin protein ligase (FBXW7) as potential targets of miR-182, and found that levels of forkhead box O3, but not FBXW7, were significantly decreased in fibrotic samples. These findings support a role for hepatic miRNAs in the pathogenesis of NAFLD-related fibrosis and yield possible new insight into the molecular mechanisms underlying the initiation and progression of liver fibrosis and cirrhosis.
MeSH term(s)	Demography ; Down-Regulation/genetics ; Female ; Gene Expression Profiling ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/complications ; Liver Cirrhosis/genetics ; Liver Cirrhosis/pathology ; Male ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Middle Aged ; Non-alcoholic Fatty Liver Disease/complications ; Non-alcoholic Fatty Liver Disease/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Real-Time Polymerase Chain Reaction ; Reproducibility of Results ; Up-Regulation/genetics
Chemical Substances	MicroRNAs ; RNA, Messenger
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2246684-8
ISSN	1878-1810 ; 1532-6543 ; 1931-5244
ISSN (online)	1878-1810 ; 1532-6543
ISSN	1931-5244
DOI	10.1016/j.trsl.2015.04.014
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