Meaning of Lagging strand medical term.

Mark Hedglin was born in Clarks Summit, PA, and received his B.A. degree in Biochemistry from Ithaca College. While at Ithaca College he performed research in the lab of Dr. Scott Ulrich, focusing on the rational design of isozyme-specific histone deacetylases (HDAC) inhibitors. He was also a member of the football team and a two-time District I Academic All-American and an ESPN Academic All-American. He obtained his Ph.D. degree in Chemical Biology at the University of Michigan under the supervision of Dr. Patrick J. O’Brien. His graduate studies focused on elucidating the searching mechanism of a human DNA repair enzyme. In 2010, his interests shifted from DNA damage repair to DNA damage tolerance and he joined the laboratory of Dr. Stephen J. Benkovic in the Department of Chemistry at the Pennsylvania State University where he was the recipient of the Ruth L. Kirschstein National Research Service Award from the National Cancer Institute of the NIH. His postdoctoral studies focus on human DNA replication and DNA damage tolerance.

Function: A building block for DNA synthesis of the lagging strand.

Coordinated Leading and Lagging Strand DNA Synthesis on a Minicircular Template ......

DNA for the lagging strand is ...

The resulting structure has two...

An Okazaki fragment is a relatively short fragment of DNA created on the lagging during DNA replication.

Leading strand Okazaki fragments Replication fork.

coli and are generally between 100 to 200 nucleotides in eukaryotes....

The assembly of the lagging strand holoenzyme is facilitated by several factors ...

Lagh ...We refer to this delayed, fragmented, daughter DNA as the lagging strand.
reason why Okazaki fragments are created during lagging strand DNA synthesis.

lagging strand replication during DNA synthesis

How can an antiparallel DNA () strand be duplicated by a that synthesises DNA in only one direction? This paradox of DNA synthesis on the lagging strand was dissolved by discovery of Okazaki fragments. The major components of the bacterial replication fork include , and . The loading of , , is the most critical step for assembly of a primosome, a protein complex responsible for duplex unwinding and primer RNA () synthesis at the replication fork. may be an asymmetric dimer, each of which may concurrently synthesise leading or lagging strand. Several different modes of primosome assembly have been identified in bacteria. At oriC (origin of chromosome), -dependent primosome is assembled for initiation of a round of DNA replication, whereas -dependent primosome is assembled at stalled replication forks to facilitate replication restart.

The whole lagging strand is synthesized by repeating steps (b) to (e).

daughter DNA that are made on the lagging strand by DNA ..

Stalled replication fork: A replication fork the movement of which is blocked by internal and external ‘replication stress’ including DNA damages and depletion of nucleotide precursors.

coli, these are 1 - 3 kb long fragments synthesized on the lagging strand.

Leading strand vs. lagging strand | Doovi

During S-phase, minor DNA damage may be overcome by DNA damage tolerance (DDT) pathways that bypass such obstacles, postponing repair of the offending damage to complete the cell cycle and maintain cell survival. In translesion DNA synthesis (TLS), specialized DNA polymerases replicate the damaged DNA, allowing stringent DNA synthesis by a replicative polymerase to resume beyond the offending damage. Dysregulation of this DDT pathway in human cells leads to increased mutation rates that may contribute to the onset of cancer. Furthermore, TLS affords human cancer cells the ability to counteract chemotherapeutic agents that elicit cell death by damaging DNA in actively replicating cells. Currently, it is unclear how this critical pathway unfolds, in particular, where and when TLS occurs on each template strand. Given the semidiscontinuous nature of DNA replication, it is likely that TLS on the leading and lagging strand templates is unique for each strand. Since the discovery of DDT in the late 1960s, most studies on TLS in eukaryotes have focused on DNA lesions resulting from ultraviolet (UV) radiation exposure. In this review, we revisit these and other related studies to dissect the step-by-step intricacies of this complex process, provide our current understanding of TLS on leading and lagging strand templates, and propose testable hypotheses to gain further insights.