Английская Википедия:Charles David Allis

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Charles David Allis (March 22, 1951 – January 8, 2023) was an American molecular biologist, and the Joy and Jack Fishman Professor at the Rockefeller University. He was also the Head of the Laboratory of Chromatin Biology and Epigenetics, and a professor at the Tri-Institutional MD–PhD Program (the other two institutions being the Memorial Sloan Kettering Cancer Center and Weill Cornell Medicine).[1]

Early life and education

Allis was born and raised in Cincinnati, Ohio. His father was a city planner and his mother an elementary school teacher.[2] He entered the University of Cincinnati in 1969, majoring in biology. He had his first experience of basic research in his senior (or fourth) year of Bachelor of Science. The experience attracted him to research, and he went to Indiana University Bloomington for graduate studies.[3] He graduated with an MSc in 1975 and a PhD three years later, under the supervision of Anthony Mahowald.[1][3]

Career

Allis undertook a postdoctoral fellowship in the University of Rochester after obtaining his PhD.[3] In 1981, he joined the Baylor College of Medicine as an assistant professor in the Department of Biochemistry and Department of Cell Biology, and was promoted to associate professor in 1986 and full professor in 1989.[1] He joined the Department of Biology at Syracuse University College of Arts and Sciences in 1990.[4]

Allis returned to the University of Rochester in 1995, and became the Marie Curran Wilson and Joseph Chamberlain Wilson Professor of Biology two years later.[5] In 1998, Allis went to the Department of Biochemistry and Molecular Genetics at the University of Virginia School of Medicine.[6] He joined the Rockefeller University in 2003 as the Joy and Jack Fishman Professor and Head of the Laboratory of Chromatin Biology and Epigenetics.[1]

Allis had been treated for cancer.[7] He died January 8, 2023, at a hospital in Seattle, Washington.[7]

Research

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Allis was known for his research of histone modifications and their relation to chromatin structure. He started working on Tetrahymena, a ciliated unicellular eukaryote. Tetrahymena is an ideal candidate to study histone acetylation due to its dual nucleus. It has a larger macronucleus that is transcriptionally active and somatic, and a smaller micronucleus that is transcriptionally silent and germline.[8] Chromatin biology at the time was not a popular topic; nor was the use of ciliated organisms.[3]

In 1996, his group isolated the histone acetyltransferase p55 from Tetrahymena, an enzyme that acetylates histones, and found the enzyme was homologous to Gcn5p, a known transcriptional co-activator in yeast.[9][10] This was the first time that histone acetyltransferases were connected to DNA transcription activation,[11] verifying Vincent Allfrey's hypothesis in the 1960s that histone acetylation regulates transcription.[12][13]

Following this seminal report, Allis continued studying histone acetylation, discovering more histone acetyltransferases, including TAF1 (part of the transcription factor TFIID needed to initiate transcription).[14] Allis also branched off to researching histone phosphorylation and histone methylation. He linked histone phosphorylation to mitosis and mitogen stimulation,[15][16] and established a synergistic relationship between histone phosphorylation and acetylation.[17] He also determined the role of methylation at lysine 9 of histone H3,[18] identified SET domain-containing proteins as histone methyltransferase,[19] and found that histone ubiquitylation regulates histone methylation.[20]

In 2000, Allis and Brian Strahl proposed the "histone code hypothesis", which states that DNA transcription is largely regulated by histone modifications.[21] Later, Allis (together with Thomas Jenuwein) explicitly associated the histone code with epigenetics,[22] and recognized the clinical significance of histone modifications, especially in cancers.[23][24]

In more recent years, his attention turned to "oncohistones", which are histones with mutations that distort normal histone modifications, leading to cancers.[25][26]

Honors and awards

Allis was a member of Phi Beta Kappa when he graduated from the University of Cincinnati.[5]

The C. David Allis Mentorship Fund for Young Scientists at the Rockefeller University was established in his honor.[44][45]

References

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