Xiro homeoproteins coordinate cell cycle exit and primary neuron formation by upregulating neuronal-fate repressors and downregulating the cell-cycle inhibitor XGadd45-γ
Author
dc.contributor.author
Calle Mustienes, Elisa de la
Author
dc.contributor.author
Glavic Maurer, Álvaro
Author
dc.contributor.author
Modolell, Juan
Author
dc.contributor.author
Gómez Skarmeta, José Luis
Admission date
dc.date.accessioned
2018-12-19T20:28:21Z
Available date
dc.date.available
2018-12-19T20:28:21Z
Publication date
dc.date.issued
2002
Cita de ítem
dc.identifier.citation
Mechanisms of Development, Volumen 119, Issue 1, 2002, Pages 69-80
Identifier
dc.identifier.issn
09254773
Identifier
dc.identifier.other
10.1016/S0925-4773(02)00296-4
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/153467
Abstract
dc.description.abstract
The iroquois (iro) homeobox genes participate in many developmental processes both in vertebrates and invertebrates, among them are
neural plate formation and neural patterning. In this work, we study in detail Xenopus Iro (Xiro) function in primary neurogenesis. We show
that misexpression of Xiro genes promotes the activation of the proneural gene Xngnr1 but suppresses neuronal differentiation. This is
probably due to upregulation of at least two neuronal-fate repressors: XHairy2A and XZic2. Accordingly, primary neurons arise at the border
of the Xiro expression domains. In addition, we identify XGadd45-g as a new gene repressed by Xiro. XGadd45-g encodes a cell-cycle
inhibitor and is expressed in territories where cells will exit mitosis, such as those where primary neurons arise. Indeed, XGadd45-g
misexpression causes cell cycle arrest. We conclude that, during Xenopus primary neuron formation, in Xiro expressing territories neuronal
differentiation is impaired, while in adjacent cells, XGadd45-g may help cells stop dividing and differentiate as neurons. q 2002 Elsevier
Science Ireland Ltd. All rights reserved.
Xiro homeoproteins coordinate cell cycle exit and primary neuron formation by upregulating neuronal-fate repressors and downregulating the cell-cycle inhibitor XGadd45-γ