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Dr. John Torday, Ph.D. is an Investigator at The Lundquist Institute of Biomedical Innovation, a Professor of Pediatrics and Obstetrics/Gynecology, and Faculty, Evolutionary Medicine, at the David Geffen School of Medicine at UCLA, and Director of the Perinatal Research Training Program, the Guenther Laboratory for Cell-Molecular Biology, and Faculty in the Division of Neonatology, at Harbor-UCLA Medical Center.

Dr. Torday studies the cellular-molecular development of the lung and other visceral organs, and using the well-established principles of cell-cell communication as the basis for determining the patterns of physiologic development, his laboratory was the first to determine the complete repertoire of lung alveolar morphogenesis. This highly regulated structure offered the opportunity to trace the evolution of the lung from its unicellular origins forward, developmentally and phylogenetically. The lung is an algorithm for understanding the evolution of other physiologic properties, such as in the kidney, skin, liver, gut, and central nervous system. Such basic knowledge of the how and why of physiologic evolution is useful in the effective diagnosis and treatment of disease.

Dr. Torday received his undergraduate degree in Biology and English from Boston University, and his MSc and PhD in Experimental Medicine from McGill University, Montreal, Canada. He did a post-doctoral Fellowship in Reproductive Endocrinology at the University of Wisconsin-Madison, WI.

Dr. Torday’s research has led to the publication of more than 150 peer-reviewed articles and 350 abstracts. More recently, he has gained an interest in the evolutionary aspects of comparative physiology and development, leading to the publication of 12 peer-reviewed articles on the cellular origins of vertebrate physiology, culminating in the book Evolutionary Biology, Cell-Cell Communication and Complex Disease.

In the search for ways to effectively combat age-related human disease, the enzyme sirtuin 6 (Sirt6) has recently become a focus of biochemical research. A targeted activation of Sirt6 could prevent or mitigate such diseases, for example some types of cancer. In a paper for the journal Nature Chemical Biology, biochemists from the University of Bayreuth have now shown how the small molecule MDL-801 binds to the enzyme Sirt6 and influences its activity. These findings stand to aid the development of new drugs.

Tissue engineering has long-depended on geometrically static scaffolds seeded with cells in the lab to create new tissues and even organs. The scaffolding material—usually a biodegradable polymer structure—is supplied with cells and the cells, if supplied with the right nutrients, then develop into tissue as the underlying scaffold biodegrades. But this model ignores the extraordinarily dynamic morphological processes that underlie the natural development of tissues. Now, researchers at the University of Illinois Chicago have developed new 4D hydrogels—3D materials that have the ability to change shape over time in response to stimuli—that can morph multiple times in a preprogrammed or on-demand manner in response to external trigger signals. In a new Advanced Science study, the UIC researchers, led by Eben Alsberg, show that these new materials may be used to help develop tissues that more closely resemble their natural counterparts, which are subject to forces that drive movement during their formation.

Some genes don’t stay in the same place in the genome. Sometimes called jumping genes or transposons, this genetic material can hop around and rearrange itself | Genetics And Genomics.


Some genetic sequences don’t stay in the same place in the genome. Sometimes called jumping genes or transposons, this genetic material can hop around and rearrange itself to create new sequences. Some transposons even encode for their own enzymes, and these co-called transposases can edit the genome by cutting sequences from one place and pasting them to another.

Reporting in Science, researchers have now suggested that transposable elements (TEs) can fuse with portions of existing genes that code for protein called exons, and get incorporated into genes in a process called exon shuffling to create novel genes that are functional, and express new proteins.

Now, Tejada-Martinez and her colleagues have studied the evolution of 1077 tumour suppressor genes (TSGs). In all, they compared the evolution of the genes in 15 mammalian species, including seven cetacean species.

Genes regulating DNA damage, tumour spread and the immune system were positively selected among the cetaceans. The team also found that cetaceans gained and lost TSGs at a rate 2.4 times higher than in other mammals.

It’s not like we’re gonna be taking whale genes and putting them into humans and making humans cancer resistant, says Lynch. But if you can find the genes that play a role in tumour suppression in other animals, and if you could figure out what they’re doing, maybe you can make a drug that mimics that for human treatment…