Bertrand, Helmut

Helmut Bertrand

Professor Emeritus

B.A., 1963, Bethel College
M.S., 1967, Ph.D., 1969, Kansas State University
Postdoctoral Fellow, 1969-1971, Albert Einstein College of Medicine,
(Yeshiva University, N.Y.)

Research

The main objective of my research program is to gain insights into the genetic and physiological regulatory processes involved in the progression of degenerative diseases elicited by mutations that diminish the respiratory efficiency of mitochondria. The syndromes that are instigated by such mutations include senescence and hypovirulence in fungi, aging in animals and plants, and several degenerative neuromuscular diseases in humans. In all cases, the symptoms are elicited by a gradual accumulation of dysfunctional mitochondria and the concomitant progressive deterioration of the respiratory capacity in the affected tissues. The fungus Neurospora crassa is used as the experimental model to investigate the genetic regulation of this process. Neurospora is the only genetically well-characterized, obligately aerobic organism in which respiratory mutants can be selected and manipulated effectively.

Like the human encephalomyopathies, fungal senescence syndromes are manifestations of the renegade proliferation of mitochondria that are rendered dysfunctional by mitochondrial DNA (mtDNA) mutations. Therefore, we have started to clone and characterize nuclear genes that protect mtDNA from mutation and regulatory genes involved with them coordination of the rate of division of mitochondria with the growth and physiological requirements of cells. The pertinent genes were identified through the selection of nuclear and mtDNA mutations that either cause instability in the mitochondrial genome, elicit the overproduction of normal mitochondria, or suppress the renegade proliferation of dysfunctional mitochondria.

My laboratory also is involved with the molecular characterization of linear and circular mitochondrial DNA plasmids that induce senescence in Neurospora by integrating into genes located on the mitochondrial chromosome. Current projects relate to replication, transcription, translation, integration, and evolutionary origin of these genetic elements and their role in the attenuation of virulence in the chestnut blight fungus Cryphonectria parasitica.