About

Sharon R. Long is the William C. Steere, Jr. - Pfizer Inc. Professor of Biological Sciences and a Professor, by courtesy, of Biochemistry at Stanford University. She received her B.S. with Honors from the California Institute of Technology, where she conducted independent studies in biochemistry in 1973. She completed her Ph.D. in Cell and Developmental Biology at Yale University in 1979, working with Ian Sussex on plant development. Her research began with postdoctoral work under Fred Ausubel, where she studied rhizobia-legume symbioses. She joined the Stanford faculty in 1982. Her primary research interests include the biochemistry, genetics, and cell biology of plant-bacterial symbiosis.

Research topics

• Biology
• Cell biology
• Genetics
• Biochemistry
• Pathology
• Internal medicine
• Medicine
• Pharmacology
• Neuroscience
• Chemistry
• Endocrinology
• Microbiology

Selected publications

• SIRT1-Dependent Neuroprotection by Resveratrol in TOCP-Induced Spinal Cord Injury: Modulation of ER Stress and Autophagic Flux

  Toxics · 2024 · 6 citations

  • Cell biology
  • Chemistry
  • Endocrinology

  This study explores the neuroprotective effects of resveratrol (Resv) against tri-o-cresyl phosphate (TOCP)-induced neurotoxicity in the spinal cord of adult hens. It is well documented that TOCP exposure causes significant neurodegeneration via mechanisms that involve endoplasmic reticulum (ER) stress and impaired autophagy. In this experiment, adult hens were assigned to one of four groups: Control, Resv, TOCP, and TOCP + Resv. The spinal cord tissues were examined through transmission electron microscopy, hematoxylin and eosin (HE) staining, Nissl staining, and Western blotting to evaluate key proteins associated with ER stress and autophagy. Additionally, RT-qPCR and immunofluorescence were employed to measure sirtuin1 (SIRT1) expression. The findings revealed that TOCP induced severe ultrastructural damage, including disrupted myelin sheaths, dilated ER, and extensive neurodegeneration, as confirmed by histological evaluations. The expression levels of GRP78, p-PERK, p-eIF2α, ATF4, CHOP, Beclin-1, P62, and LC3-II were also significantly elevated by TOCP. However, Resv treatment markedly attenuated these pathological changes by reducing ER stress, restoring autophagic flux, and upregulating SIRT1 expression, preserving spinal cord integrity. These results indicate that Resv can effectively counteract TOCP-induced neurotoxicity by modulating ER stress and autophagy, underscoring its potential as a therapeutic agent for neuroprotection.

  DOI

• A protease and a lipoprotein jointly modulate the conserved ExoR-ExoS-ChvI signaling pathway critical in Sinorhizobium meliloti for symbiosis with legume hosts

  PLoS Genetics · 2023 · 9 citations

  • Biology
  • Microbiology
  • Cell biology

  Sinorhizobium meliloti is a model alpha-proteobacterium for investigating microbe-host interactions, in particular nitrogen-fixing rhizobium-legume symbioses. Successful infection requires complex coordination between compatible host and endosymbiont, including bacterial production of succinoglycan, also known as exopolysaccharide-I (EPS-I). In S. meliloti EPS-I production is controlled by the conserved ExoS-ChvI two-component system. Periplasmic ExoR associates with the ExoS histidine kinase and negatively regulates ChvI-dependent expression of exo genes, necessary for EPS-I synthesis. We show that two extracytoplasmic proteins, LppA (a lipoprotein) and JspA (a lipoprotein and a metalloprotease), jointly influence EPS-I synthesis by modulating the ExoR-ExoS-ChvI pathway and expression of genes in the ChvI regulon. Deletions of jspA and lppA led to lower EPS-I production and competitive disadvantage during host colonization, for both S. meliloti with Medicago sativa and S. medicae with M. truncatula. Overexpression of jspA reduced steady-state levels of ExoR, suggesting that the JspA protease participates in ExoR degradation. This reduction in ExoR levels is dependent on LppA and can be replicated with ExoR, JspA, and LppA expressed exogenously in Caulobacter crescentus and Escherichia coli. Akin to signaling pathways that sense extracytoplasmic stress in other bacteria, JspA and LppA may monitor periplasmic conditions during interaction with the plant host to adjust accordingly expression of genes that contribute to efficient symbiosis. The molecular mechanisms underlying host colonization in our model system may have parallels in related alpha-proteobacteria.

  DOI

• Identification of a Novel Pyruvyltransferase Using ¹³ C Solid-State Nuclear Magnetic Resonance To Analyze Rhizobial Exopolysaccharides

  Journal of Bacteriology · 2021 · 5 citations

  Senior authorCorresponding
  • Biology
  • Biochemistry
  • Genetics

  gene mutant revealed a novel pyruvyltransferase that modifies galactoglucan. Few EPS pyruvyltransferases have been characterized. Our work provides insight into the biosynthesis of an important S. meliloti EPS and expands the knowledge of enzymes that modify polysaccharides.

  DOI

Recent grants

• NIH Grant R01GM030962

  NIH · $1.6M · 1993

• RoL: Regulation of cell envelope homeostasis in the alpha-proteobacterium Sinorhizobium meliloti

  NSF · $2.0M · 2020–2024

• NIH Grant R37GM030962

  NIH · $3.3M · 2004

• EAGER: Development of a Novel Genetic Screen for Plant Mutants in Medicago-Sinorhizobium Signaling

  NSF · $300k · 2011–2013

• Control of Symbiotic Gene Expression in Sinorhizobium meliloti

  NIH · $7.0M · 2010–2019

Frequent coauthors

• Giles Oldroyd

  University of Cambridge

  156 shared

• Péter Kaló

  Magyar Agrár- és Élettudományi Egyetem

  78 shared

• G. B. Kiss

  78 shared

• Jean Dénarié

  Interactions Arbres-Microorganismes

  73 shared

• Raka M. Mitra

  Gillies McIndoe Research Institute

  72 shared

• R. Varma Penmetsa

  Plant (United States)

  71 shared

• Douglas R. Cook

  University of California, Davis

  69 shared

• John F. Marsh

  John Innes Centre

  60 shared

Education

• Postdoctoral Fellow, Cell, Molecular, and Developmental Biology

  Harvard University

  1979

• Ph.D., Biology

  Yale University

  1979

• Bachelor of Science with honors

  California Institute of Technology

  1973

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