Yuna's journey to the fox land
Yuna was born in Houston, Texas, in January 2010. Yuna's name means 'snow' in one of old Korean dialects as she was born in winter. And there was actually a flurry of snow in Houston when she was born, which was quite unusual in Houston.
Yuna’s mom and dad were both professors at Baylor College of Medicine studying gene regulation. Around the time Yuna was born, they moved to Oregon Health & Science University in Portland. Yuna's mom and dad have been studying gene regulation in context of brain development and metabolism, respectively.
Yuna's mom, as a neurodevelopmental biologist, used to mention about an interesting gene, named FOXG1, whose deletion in the mouse would lead to the absence of forebrain. Yuna's early years were extremely difficult for her family as she went through inconsolable crying, seizures, frequent infections and sleep difficulties. Yuna would not have survived if there were not her grand parents, who took great care of her and prayed for her all the time. When Yuna reached almost two years old, her parents finally learned that Yuna has a mutation in the FOXG1 gene, a huge irony in life. This disorder used to be called congenital Rett syndrome as it has a lot of similar symptoms, and it is now named FOXG1 syndrome. This is a newly recognized autism spectrum disorder with less than a few hundred patients over the world but the number is expected to increase as diagnostic measure will be in place in more countries.
FOXG1 controls gene expression, and therefore it was kind of a remarkable coincidence that both her parents have perfect scientific and personal qualifications to study the FOXG1 gene.
Yuna’s mom (with dad's contribution as well) is now completely committed to fighting this disorder by studying the exact ways that this FOXG1 protein works while our brain develops, with strong translational mind to utilize their lab findings to actual treatment.
What your Donation Supports
The donation will help Soo Lee to perform several vital lines of works that are required to understand the exact mechanisms by which mutations in FOXG1 result in FOXG1 syndrome.
- Construction of additional mouse lines that recapitulate different aspects of FOXG1 syndrome.
- Investigation of FOXG1 mouse models for neurobehavioral traits, which will be integrated with the mechanistic studies.
- Establish new chemical and genetic models to screen small molecules that can restore FOXG1 function and discover lead chemicals, which can be further developed to treatment.