Michael W. Young | |
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.jpg) Michael W. Young in Nobel Prize press conference in Stockholm, December 2017 | |
| Born | Michael Warren Young (1949-03-28)March 28, 1949 (age 76) Miami, Florida, U.S. |
| Education | University of Texas, Austin (BA,PhD[1]) |
| Known for | Circadian rhythms |
| Awards | Nobel Prize in Physiology or Medicine2017 Canada Gairdner International Award2012 Wiley Prize in Biomedical Sciences2013 Shaw Prize2013 Massry Prize2012 Louisa Gross Horwitz Prize2011 Gruber Prize in Neuroscience2009 |
| Scientific career | |
| Fields | Chronobiology Biology |
| Institutions | University of Texas, Austin Stanford University School of Medicine Rockefeller University |
| Thesis | Non-essential sequences, genes, and the polytene chromosome bands of drosophila melanogaster (1975) |
| Doctoral advisor | Burke Judd |
| Doctoral students | Leslie B. Vosshall |
Michael Warren Young (born March 28, 1949) is an Americanbiologist andgeneticist. He has dedicated decades to research studying genetically controlled patterns of sleep and wakefulness withinDrosophila melanogaster.[2]
AtRockefeller University, his lab has made significant contributions in the field of chronobiology by identifying key genes associated with regulation of the internal clock responsible forcircadian rhythms. He was able to elucidate the function of theperiod gene, which is necessary for the fly to exhibit normal sleep cycles. Young's lab is also attributed with the discovery of thetimeless anddoubletime genes, which makes proteins that are also necessary for circadian rhythm. He was awarded the 2017Nobel Prize in Physiology or Medicine along withJeffrey C. Hall andMichael Rosbash "for their discoveries of molecular mechanisms controlling the circadian rhythm".[3][4]
Michael W. Young was born inMiami, Florida, on March 28, 1949.[5] His father worked forOlin Mathieson Chemical Corporation managing aluminum ingot sales for the south eastern United States. His mother worked for a law firm as a secretary. Despite no history of science or medicine in either of their backgrounds, Young’s parents were supportive of his interest in science and provided the means of scientific exploration through microscopes and telescopes. They lived in an environment close to private zoos, where occasionally some of the animals would escape into their backyard and spark Young's scientific interest.[6]
Michael Young grew up in and around Miami, Florida.[2] Then, his family moved nearDallas, Texas, where he graduated fromL. D. Bell High School.[7] In his early teens, Michael’s parents gifted him one of Darwin’s books on evolution and biological mysteries. The book described biological clocks as the reason why a strange plant he had seen years earlier produced flowers that closed during the day and opened at night. The location and composition of these clocks were unknown, and this sparked Michael Young’s interest at an early age.[6]
While working as a graduate student at theUniversity of Texas at Austin, Michael Young met his future wife Laurel Eckhardt. Later, both moved toStanford University, where Michael worked as a postdoctoral fellow and Laurel pursued her PhD withLen Herzenberg. Today, she is a Professor of Biology atHunter College. Michael and Laurel still work close to each other. Together, they have two daughters, Natalie and Arissa.[6]
Young earned his undergraduate degree inbiology fromUniversity of Texas at Austin in 1971.[2] After a summer of research with Burke Judd on theDrosophilagenome, Young stayed at the UT to complete aPh.D. ingenetics in 1975.[5] It was during his time here that Young became fascinated with research focused onDrosophila.[6] During hisgraduate work, he learned ofRon Konopka andSeymour Benzer’s work withDrosophilacircadian mutants, which led to his future work in cloning theperiod gene.[6]
Michael Young continued his studies throughpostdoctoral training atStanford University School of Medicine with an interest inmolecular genetics and particular focus on transposable elements.[2] He worked inDave Hogness’ lab and became familiar with the methods ofrecombinant DNA.[6] Two years later, he joinedRockefeller University as an assistant professor. From 1978 on he was involved in the University, serving as associate professor in 1984 and later named professor in 1988.[8] In 2004, Young was appointed Vice President for Academic Affairs and was also granted the Richard and Jeanne Fisher Chair.[5]
At The Rockefeller University in the early 1980s, Young and his two lab members, Ted Bargiello and Rob Jackson, further investigated the circadianperiod gene in Drosophila. They constructed segments of recombinant Drosophila DNA, amplified them in bacteria, and injected them inper mutant animals. A locomotor behavior monitor was used to assay behavioral activity. The team watched and recorded fly activity through the day and night to show that the fly restored circadian behavioral rhythms by transferring a functionalper gene.[9] Later, by determining the sequence of the gene on the X chromosome, they found that the arrhythmic mutation produced a functionless protein, while long-period and short-period mutants of per changed the amino acid sequence of a still functional protein.[10][11]
Following the discovery ofper, the Young lab looked for additional circadian genes. In late 1980s,Amita Sehgal,Jeff Price, Bernice Man helped Young useforward genetics to screen for additional mutations that altered fly rhythms. A new gene located on chromosome 2 was namedtimeless (tim) and was successfullycloned andsequenced. They found strong functional connections betweentim andper.Tim mutants interfered withper mRNA cycling. In 1994,Leslie Vosshall, a graduate student in Young's lab, discovered that if PER proteins were protected fromdegradation, they would accumulate without TIM, but could not move to the nuclei. Later Young and others found that TIM proteins did not accumulate in nuclei inper mutants. They concluded that PER and TIM worked together.[12] Another lab member Lino Saez, saw that PER and TIM associate with each other to stabilize each other and to allow their nuclear accumulation.[13] Later studies by the Young, Sehgal, and Edery labs revealed that light causes the rapid degradation of TIM and resets of the phase of the circadian rhythm.[14][15]
In 1998, Jeff Price from the Young lab discovered a kinase calleddoubletime (Casein kinase 1) that phosphorylates PER on certainserine residues. This signal marks it for degradation. When PER and TIM are bound, doubletime does not seem to be able tophosphorylate PER, allowing it to accumulate.[16]Young’s discovery of doubletime mutants in 1998 was soon followed by the 2001 discovery of a form ofFamilial Advanced Sleep Phase Syndrome (FASPS) in humans, which is linked to an hPer2 polymorphism that removes a serine normally phosphorylated by Casein kinase 1.[17] Other forms of FASPS are caused by mutations that alter the Casein kinase 1 gene. Doubletime mutations in Drosophila alter the phosphorylation and degradation of PER protein. This affects the regularity in period of the organism. This discovery solidified doubletime as a necessary part of the circadian clock.[18]
including the Nobel Lecture 7 December 2017Time Travels: A 40 Year Journey from Drosophila’s Clock Mutants to Human Circadian Disorders| International | |
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