Arsenite Exposure Displaces Zinc from ZRANB2 Leading to Altered Splicing

Exposure to arsenic, a class I carcinogen, affects 200 million people globally. Skin is the major target organ, but the molecular etiology of arsenic-induced skin carcinogenesis remains unclear. Arsenite (As )-induced disruption of alternative splicing could be involved, but the mechanism is unknown...

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Published inChemical research in toxicology Vol. 33; no. 6; pp. 1403 - 1417
Main Authors Banerjee, Mayukh, Ferragut Cardoso, Ana P, Lykoudi, Angeliki, Wilkey, Daniel W, Pan, Jianmin, Watson, Walter H, Garbett, Nichola C, Rai, Shesh N, Merchant, Michael L, States, J Christopher
Format Journal Article
LanguageEnglish
Published United States 15.06.2020
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Abstract Exposure to arsenic, a class I carcinogen, affects 200 million people globally. Skin is the major target organ, but the molecular etiology of arsenic-induced skin carcinogenesis remains unclear. Arsenite (As )-induced disruption of alternative splicing could be involved, but the mechanism is unknown. Zinc finger proteins play key roles in alternative splicing. As can displace zinc (Zn ) from C3H1 and C4 zinc finger motifs (zfm's), affecting protein function. ZRANB2, an alternative splicing regulator with two C4 zfm's integral to its structure and splicing function, was chosen as a candidate for this study. We hypothesized that As could displace Zn from ZRANB2, altering its structure, expression, and splicing function. As /Zn binding and mutual displacement experiments were performed with synthetic apo-peptides corresponding to each ZRANB2 zfm, employing a combination of intrinsic fluorescence, ultraviolet spectrophotometry, zinc colorimetric assay, and liquid chromatography-tandem mass spectrometry. ZRANB2 expression in HaCaT cells acutely exposed to As (0 or 5 μM, 0-72 h; or 0-5 μM, 6 h) was examined by RT-qPCR and immunoblotting. ZRANB2-dependent splicing of TRA2B mRNA, a known ZRANB2 target, was monitored by reverse transcription-polymerase chain reaction. As bound to, as well as displaced Zn from, each zfm. Also, Zn displaced As from As -bound zfm's acutely, albeit transiently. As exposure induced ZRANB2 protein expression between 3 and 24 h and at all exposures tested but not ZRANB2 mRNA expression. ZRANB2-directed TRA2B splicing was impaired between 3 and 24 h post-exposure. Furthermore, ZRANB2 splicing function was also compromised at all As exposures, starting at 100 nm. We conclude that As exposure displaces Zn from ZRANB2 zfm's, changing its structure and compromising splicing of its targets, and increases ZRANB2 protein expression as a homeostatic response both at environmental/toxicological exposures and therapeutically relevant doses.
AbstractList Exposure to arsenic, a class I carcinogen, affects 200 million people globally. Skin is the major target organ, but the molecular etiology of arsenic-induced skin carcinogenesis remains unclear. Arsenite (As )-induced disruption of alternative splicing could be involved, but the mechanism is unknown. Zinc finger proteins play key roles in alternative splicing. As can displace zinc (Zn ) from C3H1 and C4 zinc finger motifs (zfm's), affecting protein function. ZRANB2, an alternative splicing regulator with two C4 zfm's integral to its structure and splicing function, was chosen as a candidate for this study. We hypothesized that As could displace Zn from ZRANB2, altering its structure, expression, and splicing function. As /Zn binding and mutual displacement experiments were performed with synthetic apo-peptides corresponding to each ZRANB2 zfm, employing a combination of intrinsic fluorescence, ultraviolet spectrophotometry, zinc colorimetric assay, and liquid chromatography-tandem mass spectrometry. ZRANB2 expression in HaCaT cells acutely exposed to As (0 or 5 μM, 0-72 h; or 0-5 μM, 6 h) was examined by RT-qPCR and immunoblotting. ZRANB2-dependent splicing of TRA2B mRNA, a known ZRANB2 target, was monitored by reverse transcription-polymerase chain reaction. As bound to, as well as displaced Zn from, each zfm. Also, Zn displaced As from As -bound zfm's acutely, albeit transiently. As exposure induced ZRANB2 protein expression between 3 and 24 h and at all exposures tested but not ZRANB2 mRNA expression. ZRANB2-directed TRA2B splicing was impaired between 3 and 24 h post-exposure. Furthermore, ZRANB2 splicing function was also compromised at all As exposures, starting at 100 nm. We conclude that As exposure displaces Zn from ZRANB2 zfm's, changing its structure and compromising splicing of its targets, and increases ZRANB2 protein expression as a homeostatic response both at environmental/toxicological exposures and therapeutically relevant doses.
Exposure to arsenic, a class I carcinogen, affects 200 million people globally. Skin is the major target organ but the molecular etiology of arsenic-induced skin carcinogenesis remains unclear. As 3+ -induced disruption of alternative splicing could be involved, but the mechanism is unknown. Zinc finger proteins play key roles in alternative splicing. Arsenite (As 3+ ) can displace zinc (Zn 2+ ) from C3H1 and C4 zinc finger motifs (zfms), affecting protein function. ZRANB2, an alternative splicing regulator with two C4 zfms integral to its structure and splicing function was chosen as a candidate for this study. We hypothesized that As 3+ could displace Zn 2+ from ZRANB2 altering its structure, expression and splicing function. As 3+ /Zn 2+ binding and mutual displacement experiments were performed with synthetic apo-peptides corresponding to each ZRANB2 zfm, employing a combination of intrinsic fluorescence, UV spectrophotometry, zinc colorimetric assay and liquid chromatography-tandem mass spectrometry. ZRANB2 expression in HaCaT cells acutely exposed to As 3+ (0 or 5 μM; 0-72 h, or 0-5 μM; 6 h) was examined by RT-qPCR and immunoblotting. ZRANB2-dependent splicing of TRA2B mRNA, a known ZRANB2 target, was monitored by RT-PCR. As 3+ bound to, as well as displaced Zn 2+ from, each zfm. Also, Zn 2+ displaced As 3+ from As 3+ -bound zfms acutely, albeit transiently. As 3+ exposure induced ZRANB2 protein expression between 3-24 h and at all exposures tested, but not ZRANB2 mRNA expression. ZRANB2-directed TRA2B splicing was impaired between 3-24 h post-exposure. Furthermore, ZRANB2 splicing function was also compromised at all As 3+ exposures, starting at 100 nm. We conclude that As 3+ exposure displaces Zn 2+ from ZRANB2 zfms, changing its structure and compromising splicing of its targets, and increases ZRANB2 protein expression as a homeostatic response both at environmental/toxicological exposures and therapeutically relevant doses.
Author States, J Christopher
Pan, Jianmin
Wilkey, Daniel W
Watson, Walter H
Ferragut Cardoso, Ana P
Banerjee, Mayukh
Lykoudi, Angeliki
Rai, Shesh N
Garbett, Nichola C
Merchant, Michael L
AuthorAffiliation Ɨ James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA
Division of Nephrology & Hypertension, Department of Medicine, University of Louisville, Louisville, KY, USA
Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY, USA
Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, University of Louisville, Louisville, KY, USA
Biostatistics and Bioinformatics Facility, James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA
Department of Bioinformatics and Biostatistics, University of Louisville, Louisville, KY, USA
Division of Medical Oncology and Hematology, Department of Medicine, University of Louisville, Louisville, KY, USA
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  doi: 10.1016/j.taap.2017.05.031
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Snippet Exposure to arsenic, a class I carcinogen, affects 200 million people globally. Skin is the major target organ, but the molecular etiology of arsenic-induced...
Exposure to arsenic, a class I carcinogen, affects 200 million people globally. Skin is the major target organ but the molecular etiology of arsenic-induced...
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Title Arsenite Exposure Displaces Zinc from ZRANB2 Leading to Altered Splicing
URI https://www.ncbi.nlm.nih.gov/pubmed/32274925
https://pubmed.ncbi.nlm.nih.gov/PMC7405655
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