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allied
academies
Joint Event
February 21-22, 2019 | Paris, France
Microbiology & Applied
Microbiology
2
nd
International Conference on
World Congress on
Wound Care, Tissue Repair
and Regenerative Medicine
&
Journal of Trauma and Critical Care | Volume 3
The centers of premeltons signal the beginning and ends of genes
Henry M Sobell
University of Rochester, USA
P
remeltons are examples of emergent structures (i.e.,
structural solitons) that arise spontaneously in DNA due
to the presence of nonlinear excitations in its structure. They
are of two kinds: B-B (or A-A) premeltons form at specific
DNA-regions to nucleate site-specific DNA melting. These are
stationary and, being globally nontopological, undergo breather
motions that allow drugs and dyes to intercalate into DNA. B-A
(or A-B) premeltons, on the other hand, are mobile and being
globally topological, act as phase-boundaries transforming B-
into A- DNA during the structural phase-transition. They are
not expected to undergo breather-motions. A key feature of
both types of premeltons is the presence of an intermediate
structural-form in their central regions (proposed as being a
transition-state intermediate in DNA-melting and in the B- to
A- transition), which differs from either A- or B- DNA. Called
beta-DNA, this is both metastable and hyperflexible-and
contains an alternating sugar-puckering pattern along the
polymer-backbone combined with the partial-unstacking (in
its lower energy-forms) of every other base-pair. Beta-DNA is
connected to either B- or toA- DNAon either side by boundaries
possessing a gradation of nonlinear structural-change, these
being called the kink and the antikink regions. The presence
of premeltons in DNA leads to a unifying theory to understand
much of DNA physical-chemistry and molecular-biology. In
particular, premeltons are predicted to define the 5’ and 3’
ends of genes in naked-DNA and DNA in active-chromatin,
this having important implications for understanding physical
aspects of the initiation, elongation and termination of RNA-
synthesis during transcription. For these and other reasons,
the model will be of broader interest to the general audience
working in these areas. The model explains a wide variety of
data, and carries within it a number of experimental predictions
– all readily testable – as will be described in my talk.
Speaker Biography
Henry M Sobell was born in Los Angeles, California November 7, 1935, and grew up in
Brooklyn, New York, where he attended Brooklyn Technical High School (1948-1952),
Columbia College (1952-1956) and the University of Virginia School of Medicine (1956-
1960). Instead of practicing clinical medicine, He went to the Massachusetts Institute of
Technology,Cambridge,Massachusetts,to joinProfessorAlexanderRich intheDepartment
of Biology (1960-1965) where, as a Helen Hay Whitney Postdoctoral Fellow, he learned
the technique of single-crystal X-ray analysis. He joined the Chemistry Department at the
University of Rochester, College of Arts and Sciences and was then jointly appointed to the
Department of Biophysics at the University of Rochester School of Medicine and Dentistry,
becoming a full professor in both departments (1965-1993). He is internationally renowned
for his pioneering contributions to the understanding of how the anticancer agent,
actinomycin D, binds to DNA and exerts its mechanism of action. Using the technique of
X-ray crystallography, he and his research colleague, Shri C. Jain, solved the structure of
a crystalline complex containing actinomycin and deoxyguanosine, and the information
obtained from their study led them to propose a model to understand the general features
of how actinomycin binds to DNA.
e:
sobell@localnet.comHenry M. Sobell
, J Trauma Crit Care, Volume 3
DOI: 10.4066/2591-7358-C1-003