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Article ; Online: The All of Us Research Program is an opportunity to enhance the diversity of US biomedical research.

Bianchi, Diana W / Brennan, Patricia Flatley / Chiang, Michael F / Criswell, Lindsey A / D'Souza, Rena N / Gibbons, Gary H / Gilman, James K / Gordon, Joshua A / Green, Eric D / Gregurick, Susan / Hodes, Richard J / Kilmarx, Peter H / Koob, George F / Koroshetz, Walter J / Langevin, Helene M / Lorsch, Jon R / Marrazzo, Jeanne M / Pérez-Stable, Eliseo J / Rathmell, W Kimryn /

Rodgers, Griffin P / Rutter, Joni L / Simoni, Jane M / Tromberg, Bruce J / Tucci, Debara L / Volkow, Nora D / Woychik, Rick / Zenk, Shannon N / Kozlowski, Elyse / Peterson, Rachele S / Ginsburg, Geoffrey S / Denny, Joshua C

Nature medicine

2024 Volume 30, Issue 2, Page(s) 330–333

MeSH term(s)	Humans ; Population Health ; Biomedical Research ; Mentors
Language	English
Publishing date	2024-02-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-023-02744-3
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Article ; Online: Genome-wide transcriptome profiling reveals functional networks involving the Plasmodium falciparum drug resistance transporters PfCRT and PfMDR1.

Adjalley, Sophie H / Scanfeld, Daniel / Kozlowski, Elyse / Llinás, Manuel / Fidock, David A

BMC genomics

2015 Volume 16, Page(s) 1090

Abstract: Background: The acquisition of multidrug resistance by Plasmodium falciparum underscores the need to understand the underlying molecular mechanisms so as to counter their impact on malaria control. For the many antimalarials whose mode of action relates ...

Abstract	Background: The acquisition of multidrug resistance by Plasmodium falciparum underscores the need to understand the underlying molecular mechanisms so as to counter their impact on malaria control. For the many antimalarials whose mode of action relates to inhibition of heme detoxification inside infected erythrocytes, the digestive vacuole transporters PfCRT and PfMDR1 constitute primary resistance determinants. Results: Using gene expression microarrays over the course of the parasite intra-erythrocytic developmental cycle, we compared the transcriptomic profiles between P. falciparum strains displaying mutant or wild-type pfcrt or varying in pfcrt or pfmdr1 expression levels. To account for differences in the time of sampling, we developed a computational method termed Hypergeometric Analysis of Time Series, which combines Fast Fourier Transform with a modified Gene Set Enrichment Analysis. Our analysis revealed coordinated changes in genes involved in protein catabolism, translation initiation and DNA/RNA metabolism. We also observed differential expression of genes with a role in transport or coding for components of the digestive vacuole. Interestingly, a global comparison of all profiled transcriptomes uncovered a tight correlation between the transcript levels of pfcrt and pfmdr1, extending to dozens of other genes, suggesting an intricate regulatory balance in order to maintain optimal physiological processes. Conclusions: This study provides insight into the mechanisms by which P. falciparum adjusts to the acquisition of mutations or gene amplification in key transporter loci that mediate drug resistance. Our results implicate several biological pathways that may be differentially regulated to compensate for impaired transporter function and alterations in parasite vacuole physiology.
MeSH term(s)	Computational Biology/methods ; Drug Resistance, Multiple ; Gene Amplification ; Gene Expression Profiling/methods ; Gene Expression Regulation ; Membrane Transport Proteins/genetics ; Multidrug Resistance-Associated Proteins/genetics ; Mutation ; Plasmodium falciparum/genetics ; Plasmodium falciparum/physiology ; Protozoan Proteins/genetics
Chemical Substances	Mdr1 protein, Plasmodium falciparum ; Membrane Transport Proteins ; Multidrug Resistance-Associated Proteins ; PfCRT protein, Plasmodium falciparum ; Protozoan Proteins
Language	English
Publishing date	2015-12-21
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1471-2164
ISSN (online)	1471-2164
DOI	10.1186/s12864-015-2320-8
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Article ; Online: Cortical Stimulation Concurrent With Skilled Motor Training Improves Forelimb Function and Enhances Motor Cortical Reorganization Following Controlled Cortical Impact.

Jefferson, Stephanie C / Clayton, Elyse Renee / Donlan, Nicole A / Kozlowski, Dorothy Annette / Jones, Theresa A / Adkins, DeAnna Lynn

Neurorehabilitation and neural repair

2016 Volume 30, Issue 2, Page(s) 155–158

Abstract: Background: Electrical and magnetic brain stimulation can improve motor function following stroke in humans, rats, and nonhuman primates, especially when paired with rehabilitative training (RT). Previously, we found in rodent stroke models that ... ...

Abstract	Background: Electrical and magnetic brain stimulation can improve motor function following stroke in humans, rats, and nonhuman primates, especially when paired with rehabilitative training (RT). Previously, we found in rodent stroke models that epidural electrical cortical stimulation (CS) of the ipsilesional motor cortex (MC) combined with motor RT enhances motor function and motor cortical plasticity. It was unknown whether CS following experimental traumatic brain injury (TBI) would have similar effects. Objective: To test the effects of CS combined with motor training after moderate/severe TBI on behavioral outcome and motor cortical organization. Methods: Following unilateral controlled cortical impact (CCI) over the caudal forelimb area of the MC in adult male rats, forelimb reach training was administered daily for 9 weeks concurrently with subthreshold, 100-Hz monopolar CS or no-stimulation control procedures. The rate and magnitude of behavioral improvements and changes in forelimb movement representations in the injured MC as revealed by intracortical microstimulation were measured. Results: CCI resulted in severe motor impairments persisting throughout the 9 weeks of training in both groups, but CS-treated animals had significantly greater behavioral improvements. CS also increased wrist motor cortical representation, one of the main movements used in the training task, when compared with RT alone. However, the overall recovery level was modest, leaving animals still extremely impaired. Conclusions: These data suggest that CS may be useful for improving rehabilitation efficacy after TBI but also raise the possibility that the CS parameters that are highly effective following stroke are suboptimal after moderate/severe TBI.
MeSH term(s)	Animals ; Behavior, Animal/physiology ; Brain Injuries, Traumatic/therapy ; Disease Models, Animal ; Electric Stimulation Therapy/methods ; Electric Stimulation Therapy/standards ; Male ; Motor Cortex/injuries ; Motor Cortex/physiopathology ; Neuronal Plasticity ; Rats ; Rats, Long-Evans ; Recovery of Function/physiology
Language	English
Publishing date	2016-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1491637-x
ISSN	1552-6844 ; 1545-9683 ; 0888-4390
ISSN (online)	1552-6844
ISSN	1545-9683 ; 0888-4390
DOI	10.1177/1545968315600274
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Article ; Online: The RNA uridyltransferase Zcchc6 is expressed in macrophages and impacts innate immune responses.

Kozlowski, Elyse / Wasserman, Gregory A / Morgan, Marcos / O'Carroll, Dónal / Ramirez, Nora-Guadalupe P / Gummuluru, Suryaram / Rah, Jasmine Y / Gower, Adam C / Ieong, Michael / Quinton, Lee J / Mizgerd, Joseph P / Jones, Matthew R

PloS one

2017 Volume 12, Issue 6, Page(s) e0179797

Abstract: Alveolar macrophages orchestrate pulmonary innate immunity and are essential for early immune surveillance and clearance of microorganisms in the airways. Inflammatory signaling must be sufficiently robust to promote host defense but limited enough to ... ...

Abstract	Alveolar macrophages orchestrate pulmonary innate immunity and are essential for early immune surveillance and clearance of microorganisms in the airways. Inflammatory signaling must be sufficiently robust to promote host defense but limited enough to prevent excessive tissue injury. Macrophages in the lungs utilize multiple transcriptional and post-transcriptional mechanisms of inflammatory gene expression to delicately balance the elaboration of immune mediators. RNA terminal uridyltransferases (TUTs), including the closely homologous family members Zcchc6 (TUT7) and Zcchc11 (TUT4), have been implicated in the post-transcriptional regulation of inflammation from studies conducted in vitro. In vivo, we observed that Zcchc6 is expressed in mouse and human primary macrophages. Zcchc6-deficient mice are viable and born in Mendelian ratios and do not exhibit an observable spontaneous phenotype under basal conditions. Following an intratracheal challenge with S. pneumoniae, Zcchc6 deficiency led to a modest but significant increase in the expression of select cytokines including IL-6, CXCL1, and CXCL5. These findings were recapitulated in vitro whereby Zcchc6-deficient macrophages exhibited similar increases in cytokine expression due to bacterial stimulation. Although loss of Zcchc6 also led to increased neutrophil emigration to the airways during pneumonia, these responses were not sufficient to impact host defense against infection.
MeSH term(s)	Animals ; Bronchoalveolar Lavage Fluid ; Cells, Cultured ; Humans ; Immunity, Innate/physiology ; Macrophages, Alveolar/enzymology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Pneumonia, Bacterial/immunology ; RNA Nucleotidyltransferases/genetics ; RNA Nucleotidyltransferases/metabolism ; RNA Nucleotidyltransferases/physiology ; Streptococcus pneumoniae/pathogenicity
Chemical Substances	RNA Nucleotidyltransferases (EC 2.7.7.-) ; TUT7 protein, human (EC 2.7.7.52)
Language	English
Publishing date	2017-06-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0179797
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Article ; Online: The RNA uridyltransferase Zcchc6 is expressed in macrophages and impacts innate immune responses.

Elyse Kozlowski / Gregory A Wasserman / Marcos Morgan / Dónal O'Carroll / Nora-Guadalupe P Ramirez / Suryaram Gummuluru / Jasmine Y Rah / Adam C Gower / Michael Ieong / Lee J Quinton / Joseph P Mizgerd / Matthew R Jones

PLoS ONE, Vol 12, Iss 6, p e

2017 Volume 0179797

Abstract	Alveolar macrophages orchestrate pulmonary innate immunity and are essential for early immune surveillance and clearance of microorganisms in the airways. Inflammatory signaling must be sufficiently robust to promote host defense but limited enough to prevent excessive tissue injury. Macrophages in the lungs utilize multiple transcriptional and post-transcriptional mechanisms of inflammatory gene expression to delicately balance the elaboration of immune mediators. RNA terminal uridyltransferases (TUTs), including the closely homologous family members Zcchc6 (TUT7) and Zcchc11 (TUT4), have been implicated in the post-transcriptional regulation of inflammation from studies conducted in vitro. In vivo, we observed that Zcchc6 is expressed in mouse and human primary macrophages. Zcchc6-deficient mice are viable and born in Mendelian ratios and do not exhibit an observable spontaneous phenotype under basal conditions. Following an intratracheal challenge with S. pneumoniae, Zcchc6 deficiency led to a modest but significant increase in the expression of select cytokines including IL-6, CXCL1, and CXCL5. These findings were recapitulated in vitro whereby Zcchc6-deficient macrophages exhibited similar increases in cytokine expression due to bacterial stimulation. Although loss of Zcchc6 also led to increased neutrophil emigration to the airways during pneumonia, these responses were not sufficient to impact host defense against infection.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article: A Tetracycline-Repressible Transactivator System to Study Essential Genes in Malaria Parasites

Pino, Paco / Sebastian, Sarah / Kim, EunBin Arin / Bush, Erin / Brochet, Mathieu / Volkmann, Katrin / Kozlowski, Elyse / Llinás, Manuel / Billker, Oliver / Soldati-Favre, Dominique

Cell host & microbe. 2012 Dec. 13, v. 12, no. 6

2012

Abstract: A major obstacle in analyzing gene function in apicomplexan parasites is the absence of a practical regulatable expression system. Here, we identified functional transcriptional activation domains within Apicomplexan AP2 (ApiAP2) family transcription ... ...

Abstract	A major obstacle in analyzing gene function in apicomplexan parasites is the absence of a practical regulatable expression system. Here, we identified functional transcriptional activation domains within Apicomplexan AP2 (ApiAP2) family transcription factors. These ApiAP2 transactivation domains were validated in blood-, liver-, and mosquito-stage parasites and used to create a robust conditional expression system for stage-specific, tetracycline-dependent gene regulation in Toxoplasma gondii, Plasmodium berghei, and Plasmodium falciparum. To demonstrate the utility of this system, we created conditional knockdowns of two essential P. berghei genes: profilin (PRF), a protein implicated in parasite invasion, and N-myristoyltransferase (NMT), which catalyzes protein acylation. Tetracycline-induced repression of PRF and NMT expression resulted in a dramatic reduction in parasite viability. This efficient regulatable system will allow for the functional characterization of essential proteins that are found in these important parasites.
Keywords	Plasmodium falciparum ; parasites ; transcription factors ; transcriptional activation ; viability ; Plasmodium berghei ; acylation ; essential genes ; malaria ; Toxoplasma gondii
Language	English
Dates of publication	2012-1213
Size	p. 824-834.
Publishing place	Elsevier Inc.
Document type	Article
Note	2019-12-06
ZDB-ID	2278004-X
ISSN	1931-3128
ISSN	1931-3128
DOI	10.1016/j.chom.2012.10.016
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A tetracycline-repressible transactivator system to study essential genes in malaria parasites.

Pino, Paco / Sebastian, Sarah / Kim, Eunbin Arin / Bush, Erin / Brochet, Mathieu / Volkmann, Katrin / Kozlowski, Elyse / Llinás, Manuel / Billker, Oliver / Soldati-Favre, Dominique

Cell host & microbe

2012 Volume 12, Issue 6, Page(s) 824–834

Abstract	A major obstacle in analyzing gene function in apicomplexan parasites is the absence of a practical regulatable expression system. Here, we identified functional transcriptional activation domains within Apicomplexan AP2 (ApiAP2) family transcription factors. These ApiAP2 transactivation domains were validated in blood-, liver-, and mosquito-stage parasites and used to create a robust conditional expression system for stage-specific, tetracycline-dependent gene regulation in Toxoplasma gondii, Plasmodium berghei, and Plasmodium falciparum. To demonstrate the utility of this system, we created conditional knockdowns of two essential P. berghei genes: profilin (PRF), a protein implicated in parasite invasion, and N-myristoyltransferase (NMT), which catalyzes protein acylation. Tetracycline-induced repression of PRF and NMT expression resulted in a dramatic reduction in parasite viability. This efficient regulatable system will allow for the functional characterization of essential proteins that are found in these important parasites.
MeSH term(s)	Gene Expression Regulation ; Genes, Essential ; Genes, Protozoan ; Genetics, Microbial/methods ; Molecular Biology/methods ; Plasmodium berghei/genetics ; Plasmodium falciparum/genetics ; Tetracycline/metabolism ; Toxoplasma/genetics ; Trans-Activators/biosynthesis
Chemical Substances	Trans-Activators ; Tetracycline (F8VB5M810T)
Language	English
Publishing date	2012-12-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2012.10.016
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Article ; Online: Zcchc11 uridylates mature miRNAs to enhance neonatal IGF-1 expression, growth, and survival.

Jones, Matthew R / Blahna, Matthew T / Kozlowski, Elyse / Matsuura, Kori Y / Ferrari, Joseph D / Morris, Samantha A / Powers, John T / Daley, George Q / Quinton, Lee J / Mizgerd, Joseph P

PLoS genetics

2012 Volume 8, Issue 11, Page(s) e1003105

Abstract: The Zcchc11 enzyme is implicated in microRNA (miRNA) regulation. It can uridylate let-7 precursors to decrease quantities of the mature miRNA in embryonic stem cell lines, suggested to mediate stem cell maintenance. It can uridylate mature miR-26 to ... ...

Abstract	The Zcchc11 enzyme is implicated in microRNA (miRNA) regulation. It can uridylate let-7 precursors to decrease quantities of the mature miRNA in embryonic stem cell lines, suggested to mediate stem cell maintenance. It can uridylate mature miR-26 to relieve silencing activity without impacting miRNA content in cancer cell lines, suggested to mediate cytokine and growth factor expression. Broader roles of Zcchc11 in shaping or remodeling the miRNome or in directing biological or physiological processes remain entirely speculative. We generated Zcchc11-deficient mice to address these knowledge gaps. Zcchc11 deficiency had no impact on embryogenesis or fetal development, but it significantly decreased survival and growth immediately following birth, indicating a role for this enzyme in early postnatal fitness. Deep sequencing of small RNAs from neonatal livers revealed roles of this enzyme in miRNA sequence diversity. Zcchc11 deficiency diminished the lengths and terminal uridine frequencies for diverse mature miRNAs, but it had no influence on the quantities of any miRNAs. The expression of IGF-1, a liver-derived protein essential to early growth and survival, was enhanced by Zcchc11 expression in vitro, and miRNA silencing of IGF-1 was alleviated by uridylation events observed to be Zcchc11-dependent in the neonatal liver. In neonatal mice, Zcchc11 deficiency significantly decreased IGF-1 mRNA in the liver and IGF-1 protein in the blood. We conclude that the Zcchc11-mediated terminal uridylation of mature miRNAs is pervasive and physiologically significant, especially important in the neonatal period for fostering IGF-1 expression and enhancing postnatal growth and survival. We propose that the miRNA 3' terminus is a regulatory node upon which multiple enzymes converge to direct silencing activity and tune gene expression.
MeSH term(s)	Animals ; Cell Differentiation ; DNA-Binding Proteins/deficiency ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Embryonic Development/genetics ; Gene Expression Regulation ; High-Throughput Nucleotide Sequencing ; Insulin-Like Growth Factor I/genetics ; Insulin-Like Growth Factor I/metabolism ; Liver/metabolism ; Mice ; MicroRNAs/genetics ; MicroRNAs/metabolism ; RNA, Messenger/metabolism ; Uridine/genetics ; Uridine/metabolism
Chemical Substances	DNA-Binding Proteins ; MicroRNAs ; RNA, Messenger ; mirnlet7 microRNA, mouse ; Insulin-Like Growth Factor I (67763-96-6) ; ZCCHC11 protein, mouse (EC 2.7.7.-) ; Uridine (WHI7HQ7H85)
Language	English
Publishing date	2012-11-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1003105
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