Judith Potashkin

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Judith Potashkin
Alma materState University of New York at Buffalo
Scientific career
InstitutionsRosalind Franklin University of Medicine and Science
Thesis Isolation and characterization of residual nuclei from S̲a̲c̲c̲h̲a̲r̲o̲m̲y̲c̲e̲s̲ c̲e̲r̲e̲v̲i̲s̲i̲a̲e̲  (1985)

Judith Ann Potashkin is an American professor at Rosalind Franklin University of Medicine and Science. She is best known for her research on diseases such as Parkinson's and Alzheimer's. She is an elected fellow of the American Association for the Advancement of Science.

Contents

Education and career

Potashkin has an undergraduate degree from Lehigh University (1977), and an M.S. in from Pennsylvania State University where she worked on the connection between ribosomal RNA synthesis and viruses. [1] In 1985, Potashkin earned her Ph.D. from the State University of New York at Buffalo working on residual nuclei in yeast. [2] Following her Ph.D. she was a postdoctoral scientist at Cold Spring Harbor Laboratory. She moved to Chicago Medical School in 1990 where she is a tenured professor. [3]

Research

Potashkin is known for her research on the role of RNA in neurodegenerative diseases. Her early research examined residual nuclei in Saccharomyces cerevisiae . [4] She went on to examine the genes involved in RNA splicing [5] and identified defects in RNA processing. [6] Her research on Parkinson's disease includes defining biomarkers, [7] [8] [9] characterizing dysregulated pathways, [10] and assessing the role of nutrition. [11] Her research also extends into investigations of Alzheimer's disease. [12]

Selected publications

Awards and honors

Potashkin was elected a fellow of the American Association for the Advancement of Science in 2020. [13]

Related Research Articles

Heterochromatin is a tightly packed form of DNA or condensed DNA, which comes in multiple varieties. These varieties lie on a continuum between the two extremes of constitutive heterochromatin and facultative heterochromatin. Both play a role in the expression of genes. Because it is tightly packed, it was thought to be inaccessible to polymerases and therefore not transcribed; however, according to Volpe et al. (2002), and many other papers since, much of this DNA is in fact transcribed, but it is continuously turned over via RNA-induced transcriptional silencing (RITS). Recent studies with electron microscopy and OsO4 staining reveal that the dense packing is not due to the chromatin.

Small RNA (sRNA) are polymeric RNA molecules that are less than 200 nucleotides in length, and are usually non-coding. RNA silencing is often a function of these molecules, with the most common and well-studied example being RNA interference (RNAi), in which endogenously expressed microRNA (miRNA) or exogenously derived small interfering RNA (siRNA) induces the degradation of complementary messenger RNA. Other classes of small RNA have been identified, including piwi-interacting RNA (piRNA) and its subspecies repeat associated small interfering RNA (rasiRNA). Small RNA "is unable to induce RNAi alone, and to accomplish the task it must form the core of the RNA–protein complex termed the RNA-induced silencing complex (RISC), specifically with Argonaute protein".

<i>Saccharomyces cerevisiae</i> Species of yeast

Saccharomyces cerevisiae is a species of yeast. The species has been instrumental in winemaking, baking, and brewing since ancient times. It is believed to have been originally isolated from the skin of grapes. It is one of the most intensively studied eukaryotic model organisms in molecular and cell biology, much like Escherichia coli as the model bacterium. It is the microorganism behind the most common type of fermentation. S. cerevisiae cells are round to ovoid, 5–10 μm in diameter. It reproduces by budding.

<span class="mw-page-title-main">Z-DNA</span>

Z-DNA is one of the many possible double helical structures of DNA. It is a left-handed double helical structure in which the helix winds to the left in a zigzag pattern, instead of to the right, like the more common B-DNA form. Z-DNA is thought to be one of three biologically active double-helical structures along with A-DNA and B-DNA.

<span class="mw-page-title-main">Ethyl methanesulfonate</span> Chemical compound

Ethyl methanesulfonate (EMS) is a mutagenic, teratogenic, and carcinogenic organic compound with formula C3H8SO3. It produces random mutations in genetic material by nucleotide substitution; particularly through G:C to A:T transitions induced by guanine alkylation. EMS typically produces only point mutations. Due to its potency and well understood mutational spectrum, EMS is the most commonly used chemical mutagen in experimental genetics. Mutations induced by EMS exposure can then be studied in genetic screens or other assays.

<span class="mw-page-title-main">Fungal prion</span> Prion that infects fungal hosts

A fungal prion is a prion that infects hosts which are fungi. Fungal prions are naturally occurring proteins that can switch between multiple, structurally distinct conformations, at least one of which is self-propagating and transmissible to other prions. This transmission of protein state represents an epigenetic phenomenon where information is encoded in the protein structure itself, instead of in nucleic acids. Several prion-forming proteins have been identified in fungi, primarily in the yeast Saccharomyces cerevisiae. These fungal prions are generally considered benign, and in some cases even confer a selectable advantage to the organism.

The Kozak consensus sequence is a nucleic acid motif that functions as the protein translation initiation site in most eukaryotic mRNA transcripts. Regarded as the optimum sequence for initiating translation in eukaryotes, the sequence is an integral aspect of protein regulation and overall cellular health as well as having implications in human disease. It ensures that a protein is correctly translated from the genetic message, mediating ribosome assembly and translation initiation. A wrong start site can result in non-functional proteins. As it has become more studied, expansions of the nucleotide sequence, bases of importance, and notable exceptions have arisen. The sequence was named after the scientist who discovered it, Marilyn Kozak. Kozak discovered the sequence through a detailed analysis of DNA genomic sequences.

<span class="mw-page-title-main">Capping enzyme</span>

A capping enzyme (CE) is an enzyme that catalyzes the attachment of the 5' cap to messenger RNA molecules that are in the process of being synthesized in the cell nucleus during the first stages of gene expression. The addition of the cap occurs co-transcriptionally, after the growing RNA molecule contains as little as 25 nucleotides. The enzymatic reaction is catalyzed specifically by the phosphorylated carboxyl-terminal domain (CTD) of RNA polymerase II. The 5' cap is therefore specific to RNAs synthesized by this polymerase rather than those synthesized by RNA polymerase I or RNA polymerase III. Pre-mRNA undergoes a series of modifications - 5' capping, splicing and 3' polyadenylation before becoming mature mRNA that exits the nucleus to be translated into functional proteins and capping of the 5' end is the first of these modifications. Three enzymes, RNA triphosphatase, guanylyltransferase, and methyltransferase are involved in the addition of the methylated 5' cap to the mRNA.

<span class="mw-page-title-main">TRAMP complex</span>

TRAMP complex is a multiprotein, heterotrimeric complex having distributive polyadenylation activity and identifies wide varieties of RNAs produced by polymerases. It was originally discovered in Saccharomycescerevisiae by LaCava et al., Vanacova et al. and Wyers et al. in 2005.

Anti-Saccharomyces cerevisiae antibodies (ASCAs) are antibodies against antigens presented by the cell wall of the yeast Saccharomyces cerevisiae. These antibodies are directed against oligomannose sequences α-1,3 Man n. ASCAs and perinuclear antineutrophil cytoplasmic antibodies (pANCAs) are the two most useful and often discriminating biomarkers for colitis. ASCA tends to recognize Crohn's disease more frequently, whereas pANCA tend to recognize ulcerative colitis.

<span class="mw-page-title-main">POP7</span> Protein-coding gene in the species Homo sapiens

Ribonuclease P protein subunit p20 is an enzyme that in humans is encoded by the POP7 gene.

<span class="mw-page-title-main">MED31</span> Protein-coding gene in the species Homo sapiens

Mediator of RNA polymerase II transcription subunit 31 is a protein in humans encoded by the MED31 gene. It represents subunit Med31 of the Mediator complex. The family contains the Saccharomyces cerevisiae SOH1 homologues. SOH1 is responsible for the repression of temperature sensitive growth of the HPR1 mutant and has been found to be a component of the RNA polymerase II transcription complex. SOH1 not only interacts with factors involved in DNA repair, but transcription as well. Thus, the SOH1 protein may serve to couple these two processes.

<span class="mw-page-title-main">MAF1</span> Protein-coding gene in the species Homo sapiens

Repressor of RNA polymerase III transcription MAF1 homolog is a protein that in humans is encoded by the MAF1 gene.

mIRN21 Non-coding RNA in the species Homo sapiens

microRNA 21 also known as hsa-mir-21 or miRNA21 is a mammalian microRNA that is encoded by the MIR21 gene.

Geniom RT Analyzer is an instrument used in molecular biology for diagnostic testing. The Geniom RT Analyzer utilizes the dynamic nature of tissue microRNA levels as a biomarker for disease progression. The Geniom analyzer incorporates microfluidic and biochip microarray technology in order to quantify microRNAs via a Microfluidic Primer Extension Assay (MPEA) technique.

miR-191

miR-191 is a family of microRNA precursors found in mammals, including humans. The ~22 nucleotide mature miRNA sequence is excised from the precursor hairpin by the enzyme Dicer. This sequence then associates with RISC which effects RNA interference.

<span class="mw-page-title-main">Jens Nielsen</span> Danish biologist

Jens Nielsen is the CEO of BioInnovation Institute, Copenhagen, Denmark, and professor of systems biology at Chalmers University of Technology, Gothenburg, Sweden. He is also an adjunct professor at the Technical University of Denmark. Nielsen is the most cited researcher in the field of metabolic engineering, and he is the founding president of the International Metabolic Engineering Society. He has additionally founded several biotech companies.

<span class="mw-page-title-main">Vts1</span>

Vts1 is a post-transcriptional regulator that has RNA-binding Sterile alpha motif (SAM) domain. The protein is found in Saccharomyces cerevisiae and several eukaryotes. In Saccharomyces the Vts1 impacts vesicular transport and sporulation.

<span class="mw-page-title-main">Pathway analysis</span>

Pathway is the term from molecular biology for a curated schematic representation of a well characterized segment of the molecular physiological machinery, such as a metabolic pathway describing an enzymatic process within a cell or tissue or a signaling pathway model representing a regulatory process that might, in its turn, enable a metabolic or another regulatory process downstream. A typical pathway model starts with an extracellular signaling molecule that activates a specific receptor, thus triggering a chain of molecular interactions. A pathway is most often represented as a relatively small graph with gene, protein, and/or small molecule nodes connected by edges of known functional relations. While a simpler pathway might appear as a chain, complex pathway topologies with loops and alternative routes are much more common. Computational analyses employ special formats of pathway representation. In the simplest form, however, a pathway might be represented as a list of member molecules with order and relations unspecified. Such a representation, generally called Functional Gene Set (FGS), can also refer to other functionally characterised groups such as protein families, Gene Ontology (GO) and Disease Ontology (DO) terms etc. In bioinformatics, methods of pathway analysis might be used to identify key genes/ proteins within a previously known pathway in relation to a particular experiment / pathological condition or building a pathway de novo from proteins that have been identified as key affected elements. By examining changes in e.g. gene expression in a pathway, its biological activity can be explored. However most frequently, pathway analysis refers to a method of initial characterization and interpretation of an experimental condition that was studied with omics tools or genome-wide association study. Such studies might identify long lists of altered genes. A visual inspection is then challenging and the information is hard to summarize, since the altered genes map to a broad range of pathways, processes, and molecular functions. In such situations, the most productive way of exploring the list is to identify enrichment of specific FGSs in it. The general approach of enrichment analyses is to identify FGSs, members of which were most frequently or most strongly altered in the given condition, in comparison to a gene set sampled by chance. In other words, enrichment can map canonical prior knowledge structured in the form of FGSs to the condition represented by altered genes.

Set1 is a gene that codes for Histone-lysine N-methyltransferase and H3 lysine-4 specific proteins (H3K). Set1 proteins can also be referred to as COMPASS proteins. The first H3K4 methylase, Saccharomyces cerevisiae Set1/COMPASS, is highly conserved across a multitude of phylogenies. The histone methylation facilitated by Set1 is required for cell growth and transcription silencing through the repression of RNA polymerase II. The Set1C, COMPASS Complex, also aids in transcription elongation regulation and the maintenance of telomere length.

References

  1. Potashkin, Judith Ann (1979). An investigation of a possible mechanism of stimulation of ribosomal ribonucleic acid synthesis by simian virus 40 T-antigen (Thesis). OCLC   79946151.
  2. Potashkin, Judith Ann (1985). Isolation and characterization of residual nuclei from S̲a̲c̲c̲h̲a̲r̲o̲m̲y̲c̲e̲s̲ c̲e̲r̲e̲v̲i̲s̲i̲a̲e̲ (Thesis). OCLC   14878436.
  3. "Judith A. Potashkin, PhD". Rosalind Franklin University. Retrieved 2021-11-04.
  4. Potashkin, Judith A.; Huberman, Joel A. (1986-07-01). "Characterization of DNA sequences associated with residual nuclei of Saccharomyces cerevisiae". Experimental Cell Research. 165 (1): 29–40. doi:10.1016/0014-4827(86)90530-6. ISSN   0014-4827. PMID   3519258.
  5. Potashkin, Judith; Naik, Karuna; Wentz-Hunter, Kelly (1993-10-22). "U2AF Homolog Required for Splicing in Vivo". Science. 262 (5133): 573–575. Bibcode:1993Sci...262..573P. doi:10.1126/science.8211184. PMID   8211184.
  6. Potashkin, J.; Frendewey, D. (1990-02-01). "A mutation in a single gene of Schizosaccharomyces pombe affects the expression of several snRNAs and causes defects in RNA processing". The EMBO Journal. 9 (2): 525–534. doi:10.1002/j.1460-2075.1990.tb08139.x. ISSN   0261-4189. PMC   551696 . PMID   2406130.
  7. Chen-Plotkin, Alice S.; Albin, Roger; Alcalay, Roy; Babcock, Debra; Bajaj, Vikram; Bowman, Dubois; Buko, Alex; Cedarbaum, Jesse; Chelsky, Daniel; Cookson, Mark R.; Dawson, Ted M. (2018-08-15). "Finding useful biomarkers for Parkinson's disease". Science Translational Medicine. 10 (454): eaam6003. doi:10.1126/scitranslmed.aam6003. PMC   6097233 . PMID   30111645.
  8. Santiago, Jose A.; Potashkin, Judith A. (2015-02-17). "Network-based metaanalysis identifies HNF4A and PTBP1 as longitudinally dynamic biomarkers for Parkinson's disease". Proceedings of the National Academy of Sciences. 112 (7): 2257–2262. Bibcode:2015PNAS..112.2257S. doi: 10.1073/pnas.1423573112 . ISSN   0027-8424. PMC   4343174 . PMID   25646437.
  9. Potashkin, Judith A.; Santiago, Jose A.; Ravina, Bernard M.; Watts, Arthur; Leontovich, Alexey A. (2012-08-27). "Biosignatures for Parkinson's Disease and Atypical Parkinsonian Disorders Patients". PLOS ONE. 7 (8): e43595. Bibcode:2012PLoSO...743595P. doi: 10.1371/journal.pone.0043595 . ISSN   1932-6203. PMC   3428307 . PMID   22952715.
  10. Santiago, Jose A.; Potashkin, Judith A. (2013). "Shared dysregulated pathways lead to Parkinson's disease and diabetes". Trends in Molecular Medicine. 19 (3): 176–186. doi:10.1016/j.molmed.2013.01.002. PMID   23375873.
  11. Seidl, Stacey; Santiago, Jose; Bilyk, Hope; Potashkin, Judith (2014). "The emerging role of nutrition in Parkinson's disease". Frontiers in Aging Neuroscience. 6: 36. doi: 10.3389/fnagi.2014.00036 . ISSN   1663-4365. PMC   3945400 . PMID   24639650.
  12. Santiago, Jose A.; Potashkin, Judith A. (2021-02-12). "The Impact of Disease Comorbidities in Alzheimer's Disease". Frontiers in Aging Neuroscience. 13: 631770. doi: 10.3389/fnagi.2021.631770 . ISSN   1663-4365. PMC   7906983 . PMID   33643025.
  13. "Judith Potashkin, PhD, Elected AAAS Fellow". Rosalind Franklin University. December 17, 2020. Retrieved 2021-11-04.{{cite web}}: CS1 maint: url-status (link)