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Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts | News Archive June 17, 2013

 
The APE2 protein was previously known to be involved in DNA repair of oxidative damage ,
but not to the extent revealed in this study.. The authors refer to this distinct role for APE2
as a single-strand break end resection (“SSB end resection”).





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DNA Damage Checkpoint during Oxidative Stress

Currently, antioxidants are all the rage, as “everybody knows” that reducing the amount of “reactive oxygen species”—cell-damaging molecules that are byproducts of cellular metabolism—is critical to staying healthy. What everyone doesn’t know is that our bodies already have a complex set of processes built in to handle these harmful byproducts of being alive and repair the damage they cause.

For example, few of us realize that, while our cells’ DNA is constantly being damaged by reactive oxygen species (as well as by other forces), there are also complex mechanisms that constantly assess that damage and make repairs to our fragile genetic material at least 10,000 times a day in every cell in our bodies. The vital biochemical processes by which this constant DNA repair takes place are still only partially understood because of their complexity, speed, and the difficulty of studying complex interactions within living cells. Moreover, it remains unknown how cells sense the oxidatively damaged DNA in the first place.

In an article published in the Proceedings of the National Academy of Sciences (PNAS) a research team from University of North Carolina at Charlotte announced that they had uncovered a previously unknown surveillance mechanism, known as a DNA damage checkpoint, used by cells to monitor oxidatively damaged DNA.

“DNA damage is the underlying pathology in many major human diseases, including cancers and neurodegenerative disorders such as Alzheimer’s and Parkinson’s, so arriving at a full understanding of the sophisticated mechanisms that cells usually employ to avoid such disastrous outcomes is important,” Yan noted.


Two biochemical pathways, known as ATM-Chk2 and ATR-Chk1, govern the cell’s response and repair of double-strand DNA breaks and other types of DNA damage or replication stress respectively.

The molecular mechanisms underlying the ATR-Chk1 checkpoint activation include the uncoupling of DNA helicase and polymerase activities and DNA end resection of double-strand breaks.


“The significance of what we have found is that there is a third, previously unknown trigger for ATR-Chk1 checkpoint pathway, and this novel mechanism is discovered in the context of oxidative stress,” Yan said.

In particular, Yan’s team discovered that under conditions of oxidative stress (which occurs in the presence of hydrogen peroxide) a base excision repair protein—known as APE2—plays a critical and unexpected role in the checkpoint response: single-strand DNA generation and Chk1 association.


The APE2 protein was previously known to be involved in DNA repair of oxidative damage, but not to the extent revealed in this study.. The authors refer to this distinct role for APE2 (in the single-stand DNA generation in 3’ to 5’ directio) as a single-strand break end resection (“SSB end resection”).


The study involved experiments performed with Xenopus laves (the African clawed frog, a species commonly used as a lab animal) egg extracts – an experimental system that Yan’s lab has developed for studying DNA repair and checkpoint mechanisms in a cell-free conditions.

Xenopus is useful because it is a vertebrate (and thus quite similar to humans in cell biology), and its egg cells can be easily produced and manipulated.

Yan is hopeful that this research will open new avenues to pharmacological strategies in drug development for cancer and neurodegenerative diseases.

The paper's first-author is Jeremy Willis, UNC Charlotte biology graduate student, undergraduate honors student Yogin Patel, and co-authored by undergraduate honors student Barry L. Lentz and Shan Yan, assistant professor of biology.

The article appeared in the June 10, 2013 print edition of PNAS: http://www.pnas.org/content/early/2013/06/06/1301445110.abstract. The Yan laboratory at UNC Charlotte is funded in part by the University of North Carolina at Charlotte and a National Institute of General Medical Sciences/National Institutes of Health grant, number R15GM101571.

Original press release:http://publicrelations.uncc.edu/news-events/news-releases/new-findings-regarding-dna-damage-checkpoint-mechanism-oxidative-stress