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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
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 Dec 18, 2013

 

Satellite DNA (green) is compact in a normal cell (left)
but distended in a senescent cell (right).
The study identifies a common marker of senescence that could have
important implications for aging, progeria and cancer.

Image Credit: Swanson et al., 2013

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Aging cells unravel DNA, in seniors and Progeria kids

Senescent cells are metabolically active but incapable of dividing — and are a key to preventing the spread of cancer cells. Strikingly, cells from Progeria patients suggest their arrested cells follow the same senescence as normal aging.

The study in The Journal of Cell Biology identifies a common, early marker of senescent cells that could have important implications for tumor suppression and aging-related diseases like Progeria.

Senescent cells permanently exit the cell cycle. This process can be triggered by cellular changes associated with aging, or by the stress of cancer-promoting oncogenes.

Despite the importance of senescence in aging and tumor suppression, researchers have failed to identify any distinguishing features that are common to all types of senescent cells.


However, researchers from UMass Medical School discovered that satellite DNA located at human and mouse centromeres — center points where chromosomes connect during cell division — unraveled from a normal compact state when cells entered senescence.

This unraveling — which researchers call senescence-associated distension of satellites, or SADS — occurred regardless of how senescence was induced and appeared early in the process of cell cycle decline.

Strikingly, cells from Progeria patients also formed SADS when they exited the cell cycle. This observation suggests that prematurely aging Progeria cells follow the same senescence pathway as normally aging cells.


The extensive unfolding of structures critical for cell division could thus prove key to inhibiting cell proliferation, in the context of both aging and limiting the proliferation of tumor cells.

Abstract
Epigenetic changes to chromatin are thought to be essential to cell senescence, which is key to tumorigenesis and aging. Although many studies focus on heterochromatin gain, this work demonstrates large-scale unraveling of peri/centromeric satellites, which occurs in all models of human and mouse senescence examined. This was not seen in cancer cells, except in a benign senescent tumor in vivo. Senescence-associated distension of satellites (SADS) occurs earlier and more consistently than heterochromatin foci formation, and SADS is not exclusive to either the p16 or p21 pathways. Because Hutchinson Guilford progeria syndrome patient cells do not form excess heterochromatin, the question remained whether or not proliferative arrest in this aging syndrome involved distinct epigenetic mechanisms. Here, we show that SADS provides a unifying event in both progeria and normal senescence. Additionally, SADS represents a novel, cytological-scale unfolding of chromatin, which is not concomitant with change to several canonical histone marks nor a result of DNA hypomethylation. Rather, SADS is likely mediated by changes to higher-order nuclear structural proteins, such as LaminB1.

Submitted: 13 June 2013
Accepted: 13 November 2013

Swanson, E.C., et al. 2013. J. Cell Biol. doi:10.1083/jcb.201306073

About The Journal of Cell Biology
The Journal of Cell Biology (JCB) is published by The Rockefeller University Press. All editorial decisions on manuscripts submitted are made by active scientists in conjunction with our in-house scientific editors. JCB content is posted to PubMed Central, where it is available to the public for free six months after publication. Authors retain copyright of their published works, and third parties may reuse the content for non-commercial purposes under a creative commons license. For more information, please visit http://www.jcb.org