EEOS Department - 100 Morrissey Blvd. - Boston, MA 02125

William E. Robinson  
Professor
Environmental and Aquatic Toxicology
Phone: (617) 287-7456

Fax: (617) 287-7474

Room: S-01-058

Email: william.robinson@umb.edu

Curriculum vitae

 
     
   
  • Ph.D. Biology
    Northeastern University, Boston MA (1981)
  • M.S. Biology
    Northeastern University, Boston MA (1977)
  • A.B. Biology
    Boston University, Boston MA (1970)
   
     
   
   

My research addresses functional mechanisms in aquatic toxicology, particularly those processes involved in metal uptake, depuration, sequestration and internal transport.

This work focuses on two groups of marine organisms - bivalve molluscs (mussels and clams) and tunicates (ascidians). My students, collaborating researchers and I are investigating several mechanisms (physiological, biochemical and molecular) that bivalve molluscs and tunicates utilize in response to specific metals. Ongoing and past studies have addressed metal bioavailability, detoxification and the circulatory transport of metal ion complexes in both bivalves and tunicates. We have also conducted research aimed at advancing monitoring techniques, using the biomarker approach and the marine mussel transplant approach, in Boston Harbor and regional embayments.

In our marine bivalve research, we are concentrating our efforts to better understand how metals (black dots) can be transported in the circulatory system to the kidney for storage and possible elimination. At least three possible pathways exist:

  1. hemocytes might internalize metals and shunt them to the kidney (upper route);
  2. metals in blood plasma might pass through the ultrafilter of the pericardial glands (P.G.) and reach the kidney in the primary urine (middle route); and/or
  3. metals might be transported as metal-plasma protein complexes (lower route).

Metal Transport:

In the mussel Mytilus edulis and the quahog Mercenaria mercenaria, we have recently demonstrated that it is this third pathway that is primarily resonsible for the transport of metals such as cadmium. This transport route is similar to that known to occur in human blood, but it has not been previously recognized for bivalves. In mussels, a single plasma protein, Histidine-rich Glycoprotein (HRG) accounts for the bulk of the cadmium transport and the transfer of this metal to the kidney. We have determined the mussel HRG protein sequence (based on our sequencing of the HRG cDNA), have shown that HRG binds a variety of metals in addition to Cd (Ca, Mg, Zn, Ni, Pd, Hg), and have demonstrated that HRG is present in the blood of five additional marine bivalves (based on molecular weight and crossreactivity with mussel HRG antibodies). We are currently investigating the mechanism through which HRG passes metals over to the kidney cells - a process that we hypothesize involves a glycosaminoglycan (GAG) intermediary.

Work with tunicates seeks the answer to a 90 year-old question: Why do a number of species of tunicates maintain such extremely high concentrations of highly reduced vanadium in their blood cells? Since vanadium is normally present as V(V) in oxygenated seawater, tunicates must expend energy to reduce this vanadium and store it as V(III). We have documented that these high vanadium concentrations are present in only two or three specific types of blood cells. We have also isolated and characterized a small peptide named 'tunichrome' from blood cell preparations. It was originally thought that this tunichrome was responsible for complexing the vanadium as within the blood cells, but it is now known that tunichrome and vanadium are not co-localized in the same blood cell types. Neither the tunichrome nor the vanadium are involved in oxygen transport. While we cannot rule out an immunological role for the vanadium, we currently hypothesize that the tunichrome and vanadium are involved in the formation of the 'tunic', the leathery exoskeleton of the tunicates. This process may prove to be similar to the process known to be involved in the sclerotization of insect cuticle.

Click here for more info about our studies on bivalve molluscs and on tunicates.

   
     
   
   

"Further Development of a Marine Bivalve Model for Blood Transport and Transfer Mechanisms" William E. Robinson and James Shine (Co-PIs).

We are seeking funding to examine the process whereby Cd is transferred from mussel Histidine-rich Glycoprotein (HRG) to kidney cells. Based on published work in mammalian systems, we hypothesize that the transfer involves basal mambrane-bound glycosaminoglycans (GAGs), with heparin sulfate being the most likely GAG involved. If this proves true, then we will have identified a simple, easily manipulated in vivo model for examining linked transport-transfer processes, internalization processes, and GAG cycling processes. Because disruptions in heparin sulfate cycling, changes in the amounts of GAGs, and alterations in heparinase activities have been implicated in disruptions in cross-membrane transfer that can lead to cancer metastasis, this transport-transfer process is an important area of cancer research.

Perturbations in Biomineralization lead to the onset of Epizoic Shell Disease (ESD) by an Opportunistic Bacterial Film Community - A Novel Hypothesis," William E. Robinson and Michael Shiaris (Co-PIs).

We are seeking funding to expand our investigations of metal-binding proteins into the Crustacea, by examining calcium-binding proteins in the blood of the American lobster, Homarus americanus. To date, almost nothing is known about metal-binding plasma proteins in this group. Epizootic Shell Disease (ESD) is a relatively recent disease of American lobsters that starts with the erosion of the dorsal surfaces of the cephalothorax, and in severe cases may lead to mortality and population impacts. We propose to take a radically different approach to studying the etiology of this disease. Our overall hypothesis is that interference and perturbations in biomineralization lead to the onset of epizootic shell disease (ESD) by an opportunistic bacterial film community. In effect, a remobilization of calcium leads to a "softening" of the shell and allows opportunistic bacteria to attack its protein matrix. To address this hypothesis, we will investigate the mechanism whereby Ca is transported in lobster blood, and how Ca regulation may be modified under disease conditions.

Click here for more info about our studies on bivalve molluscs and on tunicates.

   
   
   
   

Graduate courses:

  • EEOS 635: Environmental Toxicology[ (Syllabus)][Reading List]
  • EEOS 760: Aquatic Toxicology [Syllabus] [Reading List]
  • EEOS 658: Environmental Physiology (Co-taught with Dr. Robert Stevenson)
  • EEOS 697B: Environmental Risk Analysis and Management (Co-taught with Drs. Robert Bowen and Raul Lejano) [Syllabus]
  • EEOS 788: Current Issues in Toxicology [Syllabus]
  • EEOS 691B: Current Literature in Environmental Sciences: Aquatic Toxicology


Undergraduate courses:

  • EEOS 250: Todays Issues in Environmental Science [Syllabus]
  • Hon 255: Issues in Environmental Science
  • BI 446: Marine Biology (Boston College)

See the UMass Graduate Studies Bulletin and the UMass Undergraduate Catalog for course descriptions.

   
     

  • Manuscript review for journals such as Environmental Science and Technology, Environmental Toxicology and Chemistry, Marine Biology, Biological Bulletin, Marine Ecology Progress Series, Limnology and Oceanography, Archives of Environmental Contamination and Toxicology, Comparative Biochemistry and Physiology, and Journal of Shellfish Research.

  • Proposal review for NOAA/CMER, NOAA/UNH CICEET, Fisheries and Oceans Canada, DOE/EPSCOR, UNH Sea Grant, Massachusetts Bays Program, and Long Island Sound Research Fund.

For additional information on current and past graduate students click here.


 

   
   

Frank, P., K.O. Hodgson, W.E. Robinson and K. Kustin. 1998. Vanadium K-edge X-ray Absorption Spectroscopy reveals species differences within the same ascidian genera. A comparison of whole blood from Ascidia nigra and Ascidia ceratodes. J. Biol. Chem. 273: 24498-24503.

McIntosh, L.M. and W.E. RoL.M. and W.E. Robinson. 1999. Cadmium turnover in the hemocytes of Mercenaria mercenaria (L.) in relation to hemocyte turnover. Comp. Biochem. Physiol. 123C: 61-66.

Nair, P.S. and W.E. Robinson. 1999. Purification and characterization of a histidine-rich glycoprotein that binds cadmium from the blood plasma of the bivalve Mytilus edulis. Arch. Biochem. Biophys. 366: 8-14.

Nair, P.S. and W.E. Robinson. 2000. Cadmium speciation and transport in the blood of the bivalve Mytilus edulis. Mar. Environ. Res. 50: 99-102.

Nair, P.S. and W.E. Robinson. 2001a. Histidine-rich glycoprotein in the blood of the bivalve Mytilus edulis: Role in cadmium speciation and cadmium transfer to the kidney. Aquatic Toxicology 52: 133-142.

Nair, P.S. and W.E. Robinson. 2001b. Cadmium binding to a histidine-rich glycoprotein from marine mussel blood plasma: Potentiometric titration and equilibrium speciation modeling. Environ. Toxicol. Chem. 20: 1596-1604.

Frank, P., W.E. Robinson, K. Kustin and K.O. Hodgson. 2001. Unprecedented forms of vanadium observed within the blood cells of Phallusia nigra using K-edge X-ray absorption spectroscopy. J. Inorg. Biochem. 86:635-648.

Buchsbaum, R., J. Pederson and W. E. Robinson (editors). 2004. The Decline of Fisheries Resources in New England: Evaluating the Impact of Overfishing, Contamination and Habitat Degradation. MIT Sea Grant Press. 167pp.

Robinson, W.E. and J. Pederson. 2004. Contamination, habitat degradation, overfishing - An "either - or" debate? In: Buchsbaum, R., J. Pederson and W. E. Robinson (editors). 2004. The Decline of Fisheries Resources in New England: Evaluating the Impact of Overfishing, Contamination and Habitat Degradation. MIT Sea Grant Press, Chapter 1, p. 1-10.

Pederson, J. and W.E. Robinson. 2000. Management implications: Looking ahead? In: Buchsbaum, R., J. Pederson and W. E. Robinson (editors). 2004. The Decline of Fisheries Resources in New England: Evaluating the Impact of Overfishing, Contamination and Habitat Degradation. MIT Sea Grant Press, Chapter 10, p. 157-167.

Ward, T.J. and W.E. Robinson. 2005. Evolution of cadmium resistance in Daphnia magna. Environ. Toxicol. Chem. 24:2341-2349.

Abebe, A.T., S.J. Devoid, M. Sugumaran, R. Etter and W.E. Robinson. Identification and Quantification of Histidine-rich Glycoprotein (HRG) in the Blood Plasma of Six Marine Bivalves. Comp. Biochem. Physio., in press (March 2007).

Devoid, S.J., R. Etter, M. Sugumaran, G.W. Wallace and W.E. Robinson. Histidine-rich glycoprotein from the hemolymph of the marine mussel Mytilus edulis L. binds Class A, B and Borderline metals. Environ. Toxicol. Chem. In press (May 2007).

   
     

Additional Information