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Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

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The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo. Initally designed to evaluate the internet as a teaching tool for first year medical students, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than one million visitors each month.

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 Nov 21, 2013


PrimPol 'reading' a break at a DNA strand

DNA replication forks that collapse during the process of duplication lead to double-strand breaks and are a threat to genomic stability.

Polymerase is an enzyme whose central biological function is to synthesize polymers of nucleic acids. DNA polymerase and RNA polymerase assemble DNA and RNA molecules, respectively, generally by copying a DNA or RNA template strand.

Primase is one of the most error prone and slow polymerases. Primase also acts as a halting mechanism. It prevents the leading strand of DNA from outpacing the lagging strand - by halting the progression of the replication fork.

Image Credit: Molecular Cell

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Found: ancient enzyme that affects DNA repair

The enzyme PrimPol allows cells to make copies of their DNA even when damaged, and prevents breaks in the chromosomes.

Every day, the human body produces new cells to regenerate tissues and repair those that have suffered injury. Each time these cell divisions occur, cells make copies of their DNA to pass on to the resulting daughter cells. This process of copying DNA, or replication, is very delicate, as it can generate severe alterations in the DNA associated with malignant transformation or ageing.

Researchers from the Spanish National Cancer Research Centre (CNIO), led by Juan Méndez, head of the DNA Replication Group, together with Luis Blanco, from the Severo Ochoa Molecular Biology Centre (CBM-CSIC), have discovered how the protein PrimPol, an enzyme, is capable of recognising DNA lesions. It then facilitates repair during DNA copying, avoiding irreversible or lethal damage to the cells and, therefore, to the organism.

Their results are published in the online edition of the journal Nature Structural and Molecular Biology. This study represents the continuation of a prior study, published recently by the same researchers in the journal Molecular Cell, in which they described the existence and biochemical properties of the PrimPol enzyme.

DNA within the nucleus of cells carries genes, the instruction manuals that dictate how the cell works.

"DNA structure is very stable, except during replication which normally takes approximately eight hours in human cells; during that period it becomes more fragile and can break."

Juan Méndez, head of the DNA Replication Group, Spanish National Cancer Research Centre (CNIO)

These eight hours are therefore critical for cell replication. To ensure the fidelity of copying DNA, errors are found or if the DNA is damaged, repairs must be made as efficiently as possible.

Avoiding Collapse

DNA polymerases are the enzymes responsible for synthesising new DNA. "When a DNA polymerase finds an obstacle in the DNA [a chemical alteration introduced by solar ultraviolet radiation, for example], the copy is interrupted and the process stops until the error is repaired. This interruption can cause breaks in the DNA, translocations of fragments from some chromosomes to others, and even cause cell death or malignant transformation," says Méndez.

Research carried out by CNIO and CSIC demonstrates that the PrimPol enzyme prevents the copying process from being interrupted when there is damage. PrimPol recognises breaks and skips over them, leaving repair to occur when replication is complete.

In evolutionary terms, PrimPol is a very old enzyme, and similar proteins have been found in archaebacteria, one of the first life forms that inhabited the Earth.

'Millions of years ago, life conditions were more difficult [high salinity, extreme temperatures, etc.], so PrimPol has probably adapted to synthesising DNA under conditions that encouraged damage.

"In exchange, these primitive DNA polymerases are less exact than more evolved copying systems and can introduce mutations."

Juan Méndez, head of the DNA Replication Group, Spanish National Cancer Research Centre (CNIO)

The scientists anticipate that increases in mutations could have played a key role in the evolution of genomes — as well as having an impact on the ageing of cells and the development of cancer. Having identified and characterised PrimPol in human beings, researchers are already studying its role in disease development.

Abstract Nature Structural and Molecular Biology
DNA replication forks that collapse during the process of genomic duplication lead to double-strand breaks and constitute a threat to genomic stability. The risk of fork collapse is higher in the presence of replication inhibitors or after UV irradiation, which introduces specific modifications in the structure of DNA. In these cases, fork progression may be facilitated by error-prone translesion synthesis (TLS) DNA polymerases. Alternatively, the replisome may skip the damaged DNA, leaving an unreplicated gap to be repaired after replication. This mechanism strictly requires a priming event downstream of the lesion. Here we show that PrimPol, a new human primase and TLS polymerase, uses its primase activity to mediate uninterrupted fork progression after UV irradiation and to reinitiate DNA synthesis after dNTP depletion. As an enzyme involved in tolerance to DNA damage, PrimPol might become a target for cancer therapy.

Abstract Highlights Molecular Cell
PrimPol is a second human primase that is able to start DNA chains with dNTPs
Identification of PrimPol as a DNA polymerase that tolerates AP sites and 8oxoG lesions
PrimPol is located at both DNA compartments, mitochondria, and the nucleus
PRIMPOL gene silencing affects mtDNA replication

We describe a second primase in human cells, PrimPol, which has the ability to start DNA chains with deoxynucleotides unlike regular primases, which use exclusively ribonucleotides. Moreover, PrimPol is also a DNA polymerase tailored to bypass the most common oxidative lesions in DNA, such as abasic sites and 8-oxoguanine. Subcellular fractionation and immunodetection studies indicated that PrimPol is present in both nuclear and mitochondrial DNA compartments. PrimPol activity is detectable in mitochondrial lysates from human and mouse cells but is absent from mitochondria derived from PRIMPOL knockout mice. PRIMPOL gene silencing or ablation in human and mouse cells impaired mitochondrial DNA replication. On the basis of the synergy observed with replicative DNA polymerases Pol and Pol, PrimPol is proposed to facilitate replication fork progression by acting as a translesion DNA polymerase or as a specific DNA primase reinitiating downstream of lesions that block synthesis during both mitochondrial and nuclear DNA replication.

Reference article: Repriming of DNA synthesis at stalled replication forks by human PrimPol. Silvana Mourón, Sara Rodriguez-Acebes, María I. Martínez-Jiménez, Sara García-Gómez, Sandra Chocrón, Luis Blanco, Juan Méndez. Nature Structural & Molecular Biology (2013). DOI: 10.1038/nsmb.2719