Asset Details
Do you wish to reserve the book?
Conserved sleep disturbances in FOXP1 syndrome originate from developmental dysregulation of peptidergic signaling
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Conserved sleep disturbances in FOXP1 syndrome originate from developmental dysregulation of peptidergic signaling
Do you wish to request the book?
Conserved sleep disturbances in FOXP1 syndrome originate from developmental dysregulation of peptidergic signaling
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Conserved sleep disturbances in FOXP1 syndrome originate from developmental dysregulation of peptidergic signaling
2026
Overview
Sleep disturbances are among the most prevalent clinical features of FOXP1 syndrome, yet their nature and underlying mechanisms remain unclear. Here, we report that individuals with FOXP1 syndrome suffer from insomnia with sleep maintenance problems and early waking. Consistently, common variants in FOXP genes were associated with insomnia symptoms and short sleep. These sleep disturbances were recapitulated in Drosophila FoxP mutants, which exhibit severely fragmented and reduced sleep. FoxP loss also led to circadian arrhythmicity and impaired the plasticity of neuropeptide pigment dispersing factor-secreting (PDF-secreting) neurons in a non-cell-autonomous manner. FoxP was required during development for adult sleep integrity, particularly in peptidergic neurons. Transcriptomic analyses revealed a dysregulation of genes involved in peptidergic signaling, including hugin. FoxP was expressed in hugin+ neurons (afferent to PDF-secreting neurons) during development, and its knockdown in these cells was sufficient to induce sleep fragmentation. Our findings establish an evolutionarily conserved role for FOXP proteins in the peptidergic regulation of sleep.
Publisher
American Society for Clinical Investigation
Subject
/ Animals
/ Drosophila melanogaster - genetics
/ Drosophila Proteins - genetics
/ Drosophila Proteins - metabolism
/ Female
/ Forkhead Transcription Factors - genetics
/ Forkhead Transcription Factors - metabolism
/ Humans
/ Male
/ Repressor Proteins - genetics
/ Repressor Proteins - metabolism
/ Sleep Initiation and Maintenance Disorders - genetics
/ Sleep Initiation and Maintenance Disorders - metabolism
