Sir Michael Berridge | |
|---|---|
| Born | Michael John Berridge[2] (1938-10-22)22 October 1938 |
| Died | 13 February 2020(2020-02-13) (aged 81)[2] |
| Education | University College of Rhodesia and Nyasaland (Bsc) University College (PhD) |
| Known for | Cell signaling research Discovery ofinositol trisphosphate assecond messenger |
| Awards | King Faisal International Prize in Science Louis-Jeantet Prize for Medicine Knight Bachelor Canada Gairdner International Award Albert Lasker Award for Basic Medical Research Royal Medal Dr H. P. Heineken Prize for Biochemistry and Biophysics Shaw Prize in Life Science and Medicine Wolf Prize in Medicine |
| Scientific career | |
| Fields | Physiology Biochemistry |
| Institutions | University of Virginia Case Western Reserve University University of Cambridge Babraham Institute |
| Thesis | The physiology of excretion in the cotton stainer, Dysdercus fasciatus Signoret (Hemiptera, Pyrrhocoridae) (1964) |
| Doctoral advisor | Vincent Wigglesworth |
| Notable students | Antony Galione[1] |
Sir Michael John BerridgeFRS FMedSci FBPhS[4] (22 October 1938 – 13 February 2020) was a Britishphysiologist andbiochemist. He was known for his work oncell signaling, in particular the discovery thatinositol trisphosphate acts as asecond messenger, linking events at theplasma membrane with the release ofcalcium ions (Ca2+) within thecell.
Berridge was born inGatooma (nowKadoma, Zimbabwe) inSouthern Rhodesia (nowZimbabwe). His high schoolbiology teacher convinced him and his parents that he should pursue tertiary education, and he entered the newly foundedUniversity of Rhodesia and Nyasaland (nowUniversity of Zimbabwe),[5] earning hisBsc inzoology andchemistry in 1960.[6]
He became interested ininsect physiology after helping with hisphysiology professor's research ontsetse flies, and went to the United Kingdom to study withVincent Wigglesworth, regarded as the father of insect physiology, at the Department of Zoology of theUniversity of Cambridge. Berridge became a member at theGonville and Caius College, where Wigglesworth was a fellow,[5] and obtained his PhD in 1965.[7]
Initially intending to return toSouthern Rhodesia (nowZimbabwe) after his PhD, Berridge's plan was thwarted by theRhodesian Bush War. He migrated to the United States instead, joining the Department ofBiology of theUniversity of Virginia as apostdoctoral fellow.[5] A year later, he moved to theDevelopmental Biology Center ofCase Western Reserve University. He became aresearch associate underBodil Schmidt-Nielsen at the Department ofBiology of the same university in 1967.[7]
In 1969,John Treherne invited Berridge to return to theUniversity of Cambridge and join the new Unit of Invertebrate Chemistry and Physiology that he was setting up in the Department ofZoology.[5] He first joined as a senior scientific officer, and was promoted to principal scientific officer in 1972. He became a senior principal scientific officer at the Unit of Insect Neurophysiology and Pharmacology, also at the University of Cambridge, in 1978.[7]
In 1990, Berridge joined theBabraham Institute as the Deputy Chief Scientific Officer of the Laboratory of Molecular Signalling, before serving as the Head of Signalling in 1996 until retiring in 2003.[8] After retirement, Berridge was appointed as Babraham's first emeritus Babraham Fellow.[9]
Berridge was a fellow of theTrinity College of the University of Cambridge from 1972 until his death.[6]
Berridge maintained an online textbook oncell signalling, now hosted byPortland Press under theBiochemical Society.[10]
Berridge had been studyingcell signaling when he was atCase Western Reserve University, where he received advice from Theodore W. Rall, co-discoverer of thesecond messengercyclic AMP withEarl Wilbur Sutherland Jr., who had also worked at Case Western Reserve.[11] Working on thesalivary glands of ablow fly species, Berridge showed cyclic AMP produced the samephysiological effect asserotonin, dramatically increasingsaliva secretion.[12] The idea of second messenger was new at the time, and his finding supported cyclic AMP as a second messenger of serotonin.
He continued studying cyclic AMP after returning to theUniversity of Cambridge, and conducted experiments to study how serotonin and cyclic AMP affected the movement ofions, as ion concentration difference across the salivary glandepithelium controlled the movement of water across the epithelium throughosmosis. Berridge measured thedifference in electric potential across the epithelium since ions arecharged.[11]
Surprisingly, he found that serotonin and cyclic AMP produced opposite effect to ion movement. While the former reduced the transepithelial potential difference closer to zero, the latter caused an even more negative difference. This suggested cyclic AMP caused positively-charged ions to move across the epithelium from theextracellular fluid to the inside of the salivary gland (known as thelumen).[13]
Berridge suspectedcalcium ions (Ca2+) could explain the distinct electrical but similar physiological effects of serotonin and cyclic AMP. In 1971,Howard Rasmussen, one of the first researchers to recognise the role of Ca2+ as a second messenger, was on asabbatical at Cambridge.[5] He and Rasmussen worked together and found serotonin triggered the release of Ca2+ from a storage inside thecell.[14] Later, he confirmed that serotonin activated two distinct receptor system, one through cyclic AMP and the other through Ca2+.[15]
Berridge then wanted to identify the connection betweencell surface receptor activation and the release of intracellular Ca2+ from storage. He was inspired by a review article by Robert H. Michell in 1975, which proposed receptor activation caused the breakdown ofphosphatidylinositol, which in turn openedCa2+ channels on thecell membrane to allowing Ca2+ influx into cells.[16] He hypothesised phosphatidylinositol washydrolysed into a form ofinositol phosphate anddiglyceride (DAG), and the former was eventually broken down intoinositol. He appliedlithium ions to blow fly salivary glands to inhibit the conversion of inositol phosphate to inositol.
With help fromRex Malcolm Chaplin Dawson, who was studying inositol at theBabraham Institute near Cambridge, Berridge found that phosphatidylinositol was hydrolysed intoIP3 and DAG.[17] Later the same year, he confirmed IP3 released Ca2+ from the intracellular storage, which he identified as theendoplasmic reticulum.[18] This report, together withYasutomi Nishizuka's discovery that DAG was asecond messenger in its own right and could activateprotein kinase C,[19] marked the start of the field ofcalcium signaling.[20]
The Sir Michael Berridge Prize at theBabraham Institute was named in his honour and established with his endowment.[41]
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