MbrlCatalogueTitleDetail

Do you wish to reserve the book?
Insm1a-mediated gene repression is essential for the formation and differentiation of Müller glia-derived progenitors in the injured retina
Insm1a-mediated gene repression is essential for the formation and differentiation of Müller glia-derived progenitors in the injured retina
Hey, we have placed the reservation for you!
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.
You are currently in the queue to collect this book. You will be notified once it is your turn to collect the book.
Oops! Something went wrong.
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?
Insm1a-mediated gene repression is essential for the formation and differentiation of Müller glia-derived progenitors in the injured retina
Oops! Something went wrong.
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Title added to your shelf!
Title added to your shelf!
View what I already have on My Shelf.
Oops! Something went wrong.
Oops! Something went wrong.
While trying to add the title to your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Insm1a-mediated gene repression is essential for the formation and differentiation of Müller glia-derived progenitors in the injured retina
Insm1a-mediated gene repression is essential for the formation and differentiation of Müller glia-derived progenitors in the injured retina

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
How would you like to get it?
We have requested the book for you! Sorry the robot delivery is not available at the moment
We have requested the book for you!
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.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Insm1a-mediated gene repression is essential for the formation and differentiation of Müller glia-derived progenitors in the injured retina
Insm1a-mediated gene repression is essential for the formation and differentiation of Müller glia-derived progenitors in the injured retina
Journal Article

Insm1a-mediated gene repression is essential for the formation and differentiation of Müller glia-derived progenitors in the injured retina

2012
Request Book From Autostore and Choose the Collection Method
Overview
In zebrafish, retinal injury stimulates Müller glia (MG) reprograming, allowing them to generate multipotent progenitors that replace damaged cells and restore vision. Recent studies suggest that transcriptional repression may underlie these events. To identify transcriptional repressors, we compared the transcriptomes of MG and MG-derived progenitors and identified insm1a , a repressor exhibiting a biphasic pattern of expression that is essential for retina regeneration. Insm1a was found to suppress ascl1a and its own expression, and link injury-dependent ascl1a induction with the suppression of the Wnt inhibitor dickkopf ( dkk ), which is necessary for MG dedifferentiation. We also found that Insm1a was responsible for sculpting the zone of injury-responsive MG by suppressing h b - e g f a expression. Finally, we provide evidence that Insm1a stimulates progenitor cell-cycle exit by suppressing a genetic program driving progenitor proliferation. Our studies identify Insm1a as a key regulator of retina regeneration and provide a mechanistic understanding of how it contributes to multiple phases of this process. Goldman and colleagues report that the transcriptional repressor Insm1a is essential for retinal regeneration following injury in fish. Insm1a suppresses the expression of Ascl1a to promote Müller glial cells’ dedifferentiation at early stages of regeneration, and defines the regeneration zone by negatively regulating the expression of the heparin-binding EGF. It also halts the proliferation of retinal progenitors in the late stages of the process.