Welcome to The Visible Embryo
  o >
Home-- -History-- -Bibliography- -Pregnancy Timeline- --Prescription Drugs in Pregnancy- -- Pregnancy Calculator- --Female Reproductive System- -Contact
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. 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.

WHO International Clinical Trials Registry Platform

The World Health Organization (WHO) has created a new Web site to help researchers, doctors and patients obtain reliable information on high-quality clinical trials. Now you can go to one website and search all registers to identify clinical trial research underway around the world!




Pregnancy Timeline

Prescription Drug Effects on Pregnancy

Pregnancy Calculator

Female Reproductive System

Contact The Visible Embryo

News Alerts Archive

Disclaimer: The Visible Embryo web site is provided for your general information only. The information contained on this site should not be treated as a substitute for medical, legal or other professional advice. Neither is The Visible Embryo responsible or liable for the contents of any websites of third parties which are listed on this site.
Content protected under a Creative Commons License.

No dirivative works may be made or used for commercial purposes.


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

Google Search artcles published since 2007

Home | Pregnancy Timeline | News Alerts |News Archive Jul 15, 2015 

CEP63 depletion increases stem cell death in the developing mouse brain.
RIGHT image shows dying stem cells in purple. Mice are born
with microcephaly, a characteristic feature of Seckel syndrome.
Image Credit: Berta Terré, IRB Barcelona





CEP63 Gene key to brain development and fertility

Researchers studying the gene CEP63, found mutated in a rare brain disorder called Seckel syndrome, now know why it causes microcephaly, growth defects and in some cases — male infertility.

Appearing in Nature Communications, scientists at the Institute for Research in Biomedicine — the IRB Barcelona, Spain — identified molecular details about CEP63 that reveal it is involved in brain stem cell division, a key function of brain development. Furthermore, CEP63 is associated with sperm production, unknown until this research.

Rescuing microcephaly in mice

There are no treatment options for microcephaly to date. This defect in brain growth is present in several neurodevelopmental diseases in addition to Seckel Syndrome. "There are diagnostic tests for some of these kinds of pathologies that can be performed during pregnancy. But other than early detection, expectant parents are limited to two choices, either to abort or to continue with the pregnancy, being fully aware of potential outcome," explains Travis Stracker PhD, head of the Genomic Instability and Cancer Lab at IRB Barcelona. "Our research paves the way to explore therapeutic approaches for microcephaly involving the inhibition of the protein p53."

The CEP63 protein triggers death of brain stem cells exhibiting delayed cell division due to their lack of CEP63. These cells enter programmed cell death via the gene p53.

"Cell death due to mutations in CEP63 is the main cause of brain defects. When we prevent cell death by removing p53 from developing [mouse] embryos, the brain develops to its normal size."

Jens Lüders PhD, head of the Microtubule Organization Lab, Institute for Research in Biomedicine (IRB Barcelona), Barcelona, Spain.

This observation paves the way to examine whether inhibiting p53 could provide a future treatment preventing microcephaly in carriers of the CEP63 gene.

"It is too early to say we have a treatment proposal for humans because we are in the first stage of discovery. Also, a normal sized brain does not imply a functional brain. Our next goal is to test the p53 inhibitors currently available on the same mouse models and to characterise and analyse any long-term effects. Furthermore, inhibiting p53 could be harmful as this gene has many functions in normal embryonic development,"
the researchers warn.


The study also revealed that CEP63 is related to fertility in male mice. Researchers discovered the protein is involved in sperm production and, when absent, mice have severe infertility.

"We know that CEP63 depletion leads to problems during meiosis, a specialized type of cell division required for male germ cells to produce sperm."

Travis Stracker PhD, Head of the Institute for Research in Biomedicine  — IRB Barcelona, Spain.

"It is an interesting finding because in many cases, infertility is not explainable. This study provides a new molecular perspective to examine," adds Lüders.

CEP63 is a centrosomal protein that facilitates centriole duplication and is regulated by the DNA damage response. Mutations in CEP63 cause Seckel syndrome, a human disease characterized by microcephaly and dwarfism. Here we demonstrate that Cep63-deficient mice recapitulate Seckel syndrome pathology. The attrition of neural progenitor cells involves p53-dependent cell death, and brain size is rescued by the deletion of p53. Cell death is not the result of an aberrant DNA damage response but is triggered by centrosome-based mitotic errors. In addition, Cep63 loss severely impairs meiotic recombination, leading to profound male infertility. Cep63-deficient spermatocytes display numerical and structural centrosome aberrations, chromosome entanglements and defective telomere clustering, suggesting that a reduction in centrosome-mediated chromosome movements underlies recombination failure. Our results provide novel insight into the molecular pathology of microcephaly and establish a role for the centrosome in meiotic recombination.

Authors: Marko Marjanovi, Carlos Sánchez-Huertas, Berta Terré, Rocío Gómez, Jan Frederik Scheel, Sarai Pacheco, Philip A. Knobel, Ana Martínez-Marchal, Suvi Aivio, Lluis Palenzuela, Uwe Wolfrum, Peter J. McKinnon, José A. Suja, Ignasi Roig, Vincenzo Costanzo, Jens Lüders, and Travis H. Stracker

(July 2015): DOI: 10.1038/ncomms8676

The study has been financed by the "Plan Nacional" of the Ministry of Economy and Competitiveness and by the European Union programme Marie Curie Actions, through a postdoctoral grant awarded to Marko Marjanovi, first author of the study.

About IRB Barcelona
Founded in 2005 by the Government of Catalonia and the University of Barcelona, the Institute for Research in Biomedicine (IRB Barcelona) is "Severo Ochoa Centre of Excellence", since 2011. The 23 groups and seven scientific platforms are devoted to basic and applied research with the common goal of conducting multidisciplinary projects that address important biomedical problems affecting our society, with special emphasis on cancer, metastasis, Alzheimer, diabetes and rare diseases. The institute is home to more than 400 employees from 36 countries. IRB Barcelona's ultimate objective is to translate research results to the clinic and has already established three biotechnology spin-off companies to this end. This year the IRB Barcelona celebrates its tenth anniversary.

http://www.irbbarcelona.org /@IRBBarcelona / http://www.facebook.com/irbbarcelona

Return to top of page