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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 April 28, 2014

 

The left image depicts a normal nerve reaching the muscle surrounding the eye,
as compared to (on the right) an incomplete nerve failing to make contact,
a condition resulting in permanent downward gaze in both mice and humans.

Image courtesy of Jeremy Duncan




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Tracking eye mobility problems

Being unable to lift the upper eyelid, or eyes that roll down into their eye sockets, both conditions may result from “Congenital fibrosis of the extraocular muscles type 1” (CFEOM1).

Researchers at Harvard Medical School have now identified a unique swelling at the tip of the nerve stretching to the eye muscle which causes havoc early in eye development.

Elizabeth Engle, researcher at the Howard Hughes Medical Institute (HHMI), and Bernd Fritzsch, professor and departmental executive officer in the University of Iowa (UI) College of Liberal Arts and Sciences Department of Biology, began their research on the stimulation of eye muscles by nerves, or “innervation,” 20 years ago. Approximately 10 years later, Dr. Engle identified the mutated genes in several patients with the eye movement disorder CFEOM1 and subsequently developed a mouse with the same mutation in order to study the origins of the disorder.

Dr. Fritzsch and doctoral student, Jeremy Duncan, continued the research at Harvard looking for the point at which normal development of eye muscle innervation changed course into CFEOM1. To their surprise, eye muscle innervation happens very early in eye development when they observed a unique swelling in one of the nerves leading to the occular (eye) muscle.


More detailed analysis showed that the swelling came about because nerve fibers extending from the brain into the eye socket, stopped before reaching the muscle surrounding the eye.

Their data provided evidence of what was going wrong, but not what signal was being sent to stop innervation so quickly in the mutant mice and, by extension, in humans.


Further research through breeding CFEOM1 mice with other mutant mice having eye muscle innervation defects, magnified the effects of the mutation. With this finding, the scientists identified a specific mutated protein, its function, and at least some of the molecular cargo being transported that will allow normal innervation of eye muscles. This information gave them the understanding of how to block the defect.

The work is published in the April 16, 2014 print issue of the journal Neuron.

Engle, Fritzsch, and their collaborators are currently designing new approaches to rescue errant innervation in mice. In the future, their work may help families carrying the CFEOM1 genetic mutation with possible correction to normal eye development in their children.

Highlights
• CFEOM1-KIF21A mutations cause ocular dysmotility through a gain-of-function mechanism
• Developing Kif21a mutant oculomotor axons stall and form aberrant nerve branches
• CFEOM1-Kif21a mutations provide in vivo evidence of mammalian kinesin autoregulation
• Kif21a interacts with Map1b and Map1b−/− mice also develop CFEOM

Summary
The ocular motility disorder “Congenital fibrosis of the extraocular muscles type 1” (CFEOM1) results from heterozygous mutations altering the motor and third coiled-coil stalk of the anterograde kinesin, KIF21A. We demonstrate that Kif21a knockin mice harboring the most common human mutation develop CFEOM. The developing axons of the oculomotor nerve’s superior division stall in the proximal nerve; the growth cones enlarge, extend excessive filopodia, and assume random trajectories. Inferior division axons reach the orbit but branch ectopically. We establish a gain-of-function mechanism and find that human motor or stalk mutations attenuate Kif21a autoinhibition, providing in vivo evidence for mammalian kinesin autoregulation. We identify Map1b as a Kif21a-interacting protein and report that Map1b−/− mice develop CFEOM. The interaction between Kif21a and Map1b is likely to play a critical role in the pathogenesis of CFEOM1 and highlights a selective vulnerability of the developing oculomotor nerve to perturbations of the axon cytoskeleton.


The title of the Neuron paper is “Human CFEOM1 Mutations Attenuate KIF21A Autoinhibition and Cause Oculomotor Axon Stalling.”
The research was supported by a National Institutes of Health (NIH) grant to Engle and colleague Fritzsch and HHMI funding to Engle.

http://now.uiowa.edu/2014/03/researchers-track-down-cause-eye-mobility-disorder

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