Dennis G. Searcy

Professor
dsearcy@bio.umass.edu

Education
B.S., Oregon State University, 1964
Ph.D., Uiversity of California, Los Angeles, 1968

Postdoctoral
1969-1971, California Institute of Technology
1978-1979, Oxford University
1984-1985, Museum National d'Histoire Naturelle, Paris

Research Interests

Cellular Evolution and Physiology
It is widely accepted that mitochondria evolved from symbiotic bacteria, but nonetheless the exact nature of the ancient symbiosis remains in dispute. It had been assumed, by analogy with modern cells, that the host transferred fermentation products to the bacterial symbiont. But when glucose is available, bacteria use it directly, and have no use for the host, which they quickly outgrow. Presumably, the pre-mitochondrial symbiosis was not dependent upon carbohydrate exchange.

Molecular sequence data indicate that mitochondria originated from purple sulfide-oxidizing bacteria and the cytoplasm originated from sulfur-reducing Archaea. Thus, both the mitochondria and cytoplasm evolved from sulfur-specialists. We hypothesize that the initial symbiosis was between a host cell that produced H₂S and a bacterial symbiont that oxidized it.

If such an hypothesis is true, then sulfur metabolism is a primitive shared feature of all eukaryotes, and vestiges of it may still be present in modern cells. Our observations confirm that. We have found that mitochondria are avid sulfide oxidizers, and can couple the process to ATP production. That contradicts the widespread view that sulfide is simply a metabolic poison

In regard to cytoplasmic metabolism, all cells tested (animals, plants, fungi, and various protists) vigorously produced H₂S. To observe this, it is necessary to prevent mitochondrial sulfide consumption, and that was done either by removing the O₂, or by using inhibitors such as cyanide, or by cellular fractionation. In those conditions the eukaryotic cytoplasms did indeed produce H₂S. In a mitochondrion-free cytoplasmic fraction, sulfide production occurred even in aerobic condtions, and that was an unexpected, remarkable observation.

Current research involves the "Sulfidostat", an instrument designed to measure sulfide consumption at concentrations as low as 10_-12 M sulfide. That is crucial because even 1 µM sulfide can inhibit respiration, explaining why mitochondrial sulfide consumption had not been described previously.

Questions remain such as: (1) Cells can produce H₂S even without added sulfur, indicating that a reservoir of reducible sulfur exists. If so, what is its chemical nature, and how much is there? (2) What enzyme produces the H₂S, and what is the electron donor? (3) In typical eukaryotic cells, does sulfur cycle endlessly between cytoplasm and mitochondria? (4) What are the benefits of sulfur reduction? Is it a form of mineral respiration in which sulfur can substitute for O₂, at least to some degree?

Representative Publications

Searcy, D.G. and M.A. Peterson. 2004. Hydrogen sulfide consumption measured at low steady state concentrations using a Sulfidostat. Anal. Biochem. 324: 269-275.

Searcy, D.G. 2003. Metabolic integration during the evolutionary origin of mitochondria. Cell Research 13: 229-238.

Searcy, D. G. 2001. Nutritional syntrophies and consortia as models for the origin of mitochondria. In: Symbiosis: Mechanisms and Model Systems. J. Seckbach, ed., Kluwer Academic Publishers, Dordrecht. Pps. 163-183.

Yong, R. and D.G. Searcy. 2001. Hydrogen sulfide oxidation by rooster liver mitochondria. Comp. Biochem. Physiol. B 129: 129-137.

Searcy, D.G. and S.H. Lee. 1998. Sulfur reduction by human red blood cells. J. Exp. Zool. 282: 310-322.

Searcy, D.G., S.H. Lee, D. Gleeson, R. Yong, K. Abderazzaq, and G. Dowd. 1998. Mitochondrial origin by sulfur symbiosis. In: From Symbiosis to Eukaryotism - ENDOCYROBIOLOGY VII (E. Wagner et al., eds), Geneva University Press, p. 43-51.

Searcy, D.G., J.P. Whitehead, and M.J. Maroney. 1995. Interaction of Cu,Zn superoxide dismutase with hydrogen sulfide. Arch. Biochem. Biophys. 318: 251-263.

Searcy, D.G. 1992. Origins of mitochondria and chloroplasts from sulfur-based symbioses. In Origins and Evolution of Prokaryotic and Eukaryotic Cells, H. Hartman and K. Matsuno, eds., World Scientific Publishing, Singapore, pps. 47-87.

Searcy, D.G. and W.G. Hixon. 1991. Cytoskeletal origins in sulfur-metabolizing archaebacteria. BioSystems 25: 1-11 and BioSystems 29: 151-160.

Searcy, D.G. 1987. Phylogenetic and phenotypic relationships between the eukaryotic nucleocytoplasm and thermophilic archaebacteria. Ann. NY Acad. Sci. 503: 168-179.

Searcy, D.G. 1986. The Archaebacterial Histone "HTa". In: Bacterial Chromatin, C.O. Gualerzi and C.L. Pon, eds. Springer-Verlag, Berlin, pp. 175-184.

Stein, D.B. and D.G. Searcy. 1978. Physiologically important stabilization of DNA by a prokaryotic histone-like protein. Science 202: 219-221.

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