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

The Visible Embryo provides visual references for changes in fetal development throughout pregnancy and can be navigated via fetal development or maternal changes.

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
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive May 9, 2014


Brain cells were engineered to produce fluorescent green Botch protein
in the developing mouse cortex. Nuclei of cells are in blue.

Image credit: Zhikai Chi

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New type of protein found to regulate development

Researchers have figured out how the aptly named protein Botch blocks the signaling protein called Notch, which helps regulate human development.

In a report on the discovery, online April 24 in the journal Cell Reports, the scientists say they expect the work to lead to a better understanding of how a single protein, Notch, directs actions needed for the healthy development of organs as diverse as brains and kidneys.

The Johns Hopkins team says their experiments show that Botch uses a never-before-seen mechanism, replacing one chemical group with another that physically blocks the action of another enzyme.

"We knew that Botch regulated Notch, and now we know it has its own novel way of getting the job done. What's surprising is that Botch doesn't pull from the usual toolkit of enzyme mechanics."

Valina Dawson, Ph.D., professor of neuroscience, Johns Hopkins University School of Medicine's Institute for Cell Engineering, and study leader.

Notch is, in fact, a family of four proteins with nearly identical properties and actions in mice and men. The proteins, Dawson says, dwell in the membranes surrounding cells, where they act as receptors, responding to specific signals outside of the cells by starting a chain reaction of signals inside.

"There's a laundry list of things Notch does, from getting stem cells to develop into different organs to helping produce red blood cells.

"The big question is how a seemingly simple signaling system could have such different effects."

Valina Dawson, Ph.D.

The research team led by Dawson and her husband and collaborator, Ted Dawson, M.D., Ph.D., discovered Botch while looking for proteins that could protect the brain from injury. Since it was a newly found protein, they looked for answers on how Botch functions by finding other proteins with which it could interact, that search resulted in discovering Notch.

After Notch emerges from one of the cell's protein manufacturing centers, several things have to happen before it can go to work in the cell membrane. One of these is the addition of the chemical group glycine to a specific part of the protein. After that, an enzyme called furin cuts Notch near the glycine site. Botch removes the glycine from the spot where furin cuts. More surprisingly, says Dawson, Botch then replaces the glycine with another chemical group that blocks furin from getting to the cut site.

"Researchers are used to seeing enzymes change other proteins' function through common mechanisms, like adding or subtracting a phosphate group. But Botch uses a tactic that no one has reported seeing before: It lops off glycine and adds a chemical structure called 5-oxy-proline."

Valina Dawson, Ph.D.

Now that scientists know what to look for, they'll likely be able to identify other enzymes that use the same trick, Dawson says, and Botch itself may turn out to have other target proteins.

Knowing how Botch works on Notch contributes to scientists' understanding of the biochemistry of development. Dawson adds: "It may also have implications for the treatment of some leukemias linked to a mutation in the area of Notch close to the Botch-targeted glycine."

•Botch has γ-glutamyl cyclotransferase activity
•Notch is monoglycinated on the γ-glutamyl carbon of glutamate 1,669
•Botch deglycinates Notch, preventing S1 furin-like cleavage and thus Notch signaling
•Botch creates a 5-oxy-proline posttranslational modification at Notch glutamate 1,669

Botch promotes embryonic neurogenesis by inhibiting the initial S1 furin-like cleavage step of Notch maturation. The biochemical process by which Botch inhibits Notch maturation is not known. Here, we show that Botch has γ-glutamyl cyclotransferase (GGCT) activity that deglycinates Notch, which prevents the S1 furin-like cleavage. Moreover, Notch is monoglycinated on the γ-glutamyl carbon of glutamate 1,669. The deglycinase activity of Botch is required for inhibition of Notch signaling both in vitro and in vivo. When the γ-glutamyl-glycine at position 1,669 of Notch is degylcinated, it is replaced by 5-oxy-proline. These results reveal that Botch regulates Notch signaling through deglycination and identify a posttranslational modification of Notch that plays an important role in neurogenesis.

Other authors on the paper were Zhikai Chi, Sean T. Byrne, Andrew Dolinko, Maged M. Harraz, Min-Sik Kim, George Umanah, Jun Zhong, Rong Chen, Jianmin Zhang, Jinchong Xu, Li Chen and Akhilesh Pandey, all of the Johns Hopkins University School of Medicine.

The study was funded by a McKnight Endowment Fund for Neuroscience Brain Disorders Award, the National Institute of Neurological Disorders and Stroke (grant number NS40809), the National Institute on Drug Abuse (grant number DA00266) and the Maryland Stem Cell Research Fund (grant number MSCRFII-0429).

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