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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 March 19, 2014

 

Human fetal brains spanning thirteen to 21 weeks post ovulation.

Image Credit: UNSW, Australia






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The USP9X gene is critical to brain development

Research from the University of Adelaide has confirmed that the gene USP9X is linked to intellectual disability as it is critical to the earliest stages of development in the human brain.

The gene USP9X has been investigated by Adelaide researchers for more than a decade, but in recent years scientists have begun to understand its particular importance to brain development.

In a new paper published online in the American Journal of Human Genetics, an international research team led by the University of Adelaide's Robinson Research Institute explains how mutations in USP9X are associated with intellectual disability. These mutations, which can be inherited from one generation to the next, have been shown to cause disruptions to normal brain cell function.

Speaking during Brain Awareness Week, senior co-author Dr Lachlan Jolly from the University of Adelaide's Neurogenetics Research Program says the USP9X gene has shed new light on the mysteries of brain development and disability.

Dr Jolly explains that the framework for our brain's complex network of cells begins forming in the embryo. "Not surprisingly, disorders that cause changes to this network of cells - such as intellectual disabilities, epilepsy and autism - are hard to understand, and treat," Dr Jolly says.


"By looking at patients with severe learning and memory problems, we discovered a gene - called USP9X - that is involved in creating this base network of nerve cells.

"USP9X controls both the initial generation of the nerve cells from stem cells, and also their ability to connect with one another and form proper networks."

Lachlan Jolly, PhD, University of Adelaide, department of Neurogenetics Research


"This work is critical to understanding how the brain develops, and how it is altered in individuals with brain disorders," adds Jolly. "We hope that by learning more about genes such as USP9X, we will come to understand brain disorders at a much deeper level than currently known, leading to future treatment opportunities."

Abstract
With a wealth of disease-associated DNA variants being recently reported, the challenges of providing their functional characterization are mounting. Previously, as part of a large systematic resequencing of the X chromosome in 208 unrelated families with nonsyndromic X-linked intellectual disability, we identified three unique variants (two missense and one protein truncating) in USP9X. To assess the functional significance of these variants, we took advantage of the Usp9x knockout mouse we generated. Loss of Usp9x causes reduction in both axonal growth and neuronal cell migration. Although overexpression of wild-type human USP9X rescued these defects, all three USP9X variants failed to rescue axonal growth, caused reduced USP9X protein localization in axonal growth cones, and (in 2/3 variants) failed to rescue neuronal cell migration. Interestingly, in one of these families, the proband was subsequently identified to have a microdeletion encompassing ARID1B, a known ID gene. Given our findings it is plausible that loss of function of both genes contributes to the individual's phenotype. This case highlights the complexity of the interpretations of genetic findings from genome-wide investigations. We also performed proteomics analysis of neurons from both the wild-type and Usp9x knockout embryos and identified disruption of the cytoskeleton as the main underlying consequence of the loss of Usp9x. Detailed clinical assessment of all three families with USP9X variants identified hypotonia and behavioral and morphological defects as common features in addition to ID. Together our data support involvement of all three USP9X variants in ID in these families and provide likely cellular and molecular mechanisms involved.


Authors
Claire C. Homan, Raman Kumar, Lam Son Nguyen, Eric Haan, F. Lucy Raymond, Fatima Abidi, Martine Raynaud, Charles E. Schwartz, Stephen A. Wood, Jozef Gecz, and Lachlan A. Jolly


This research has been funded by the National Health and Medical Research Council (NHMRC) and the Women's and Children's Hospital Foundation.