Distinct susceptibility of developing neurons to death following Bax overexpression in the chicken embryo

Satô, Noboru; Sakuma, Chie; Sato, Yuka; Gould, Thomas W.; Oppenheim, Ronald W.; Yaginuma, Hiroyuki

doi:10.1038/sj.cdd.4401760

Cited by 7 publications

(4 citation statements)

References 38 publications

(67 reference statements)

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“…For instance, DRG neurons fail to undergo apoptosis in bax KO mice (38,53) and in vitro cultures of DRG neurons prepared from bax KO mice survived in the absence of the neurotrophic support, NGF which induces widespread apoptosis in WT cultures (37). Furthermore, loss of bax prevented death in bcl-x deficient mice (54) whereas over-expression of bax in chick embryos increases the susceptibility of sensory neurons to apoptosis (55). Given the critical role for bax in controlling death in these neurons, we hypothesize that if p53 is induced in neuronal progenitor cells or neurons when Brn-3b is elevated there will be increased apoptosis as a consequence of elevated Bax.…”

Section: Discussionmentioning

confidence: 99%

Brn-3b enhances the pro-apoptotic effects of p53 but not its induction of cell cycle arrest by cooperating in trans-activation of bax expression

Budhram-Mahadeo¹,

Bowen²,

Lee³

et al. 2006

Nucleic Acids Research

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The Brn-3a and Brn-3b transcription factor have opposite and antagonistic effects in neuroblastoma cells since Brn-3a is associated with differentiation whilst Brn-3b enhances proliferation in these cells. In this study, we demonstrate that like Brn-3a, Brn-3b physically interacts with p53. However, whereas Brn-3a repressed p53 mediated Bax expression but cooperated with p53 to increase p21cip1/waf1, this study demonstrated that co-expression of Brn-3b with p53 increases trans-activation of Bax promoter but not p21cip1/waf1. Consequently co-expression of Brn-3b with p53 resulted in enhanced apoptosis, which is in contrast to the increased survival and differentiation, when Brn-3a is co-expressed with p53. For Brn-3b to cooperate with p53 on the Bax promoter, it requires binding sites that flank p53 sites on this promoter. Furthermore, neurons from Brn-3b knock-out (KO) mice were resistant to apoptosis and this correlated with reduced Bax expression upon induction of p53 in neurons lacking Brn-3b compared with controls. Thus, the ability of Brn-3b to interact with p53 and modulate Bax expression may demonstrate an important mechanism that helps to determine the fate of cells when p53 is induced.

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Section: Discussionmentioning

confidence: 99%

Brn-3b enhances the pro-apoptotic effects of p53 but not its induction of cell cycle arrest by cooperating in trans-activation of bax expression

Budhram-Mahadeo¹,

Bowen²,

Lee³

et al. 2006

Nucleic Acids Research

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“…7 and 8), reflecting the survival signals mediated by this receptor in early development (Hernández-Sánchez et al, 2006). Furthermore, overexpression of the proapototic molecule Bax in neurulating chick embryos results in a moderate reduction in the number of RGCs at E9 (10-20%, Sato et al, 2006). Similarly, genetic deletion of Dlx1/Dlx2 in the mouse increases apoptosis at E13.5 and E16.5, as well as decreases RGC number by 34% (De Melo et al, 2005).…”

Section: Early Neural Cell Death Affecting Retinal Ganglion Cell Genementioning

confidence: 99%

Early neural cell death: numbers and cues from the developing neuroretina

Valenciano¹,

Boya²,

Rosa³

2009

Int. J. Dev. Biol.

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Programmed cell death is a well established key process required for proper development of the nervous system. The regulatory and executor mechanisms controlling survival/ death of projection neurons, as well as of other types of differentiated neurons and glial cells, have been studied intensely during neural development. Much less attention has been paid to earlier cell death events affecting neuroepithelial cells and recently born neurons and glial cells. We review here the reports on cell death during vertebrate retina development, our model system for many years, which has provided clear evidence of the importance of early neural cell death. We tentatively categorize the available observations in three death phases, namely morphogenetic cell death, early neural cell death and neurotrophic cell death. The magnitude and the precise regulation of the early phases of cell death are fully comparable to the much better characterized neurotrophic cell death. Therefore, early neural cell death deserves a profound dedicated study; this will help to obtain an integrated understanding of the development of the retina and other parts of the vertebrate nervous system.

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“…In ovo electroporation was performed as described previously (Sato et al, 2006), with slight modifications. Details are described in the supplementary Materials and Methods.…”

Section: In Ovo Electroporationmentioning

confidence: 99%

“…Several previous studies, including our own, have clarified several characteristics of this neuronal death within the cervical spinal cord. The degenerating MNs show the morphological features of apoptosis, as well as activation of caspase proteins, indicating that these MNs die by apoptosis (O'Connor and Wyttenbach, 1974;Sato et al, 2006;Yaginuma et al, 1996Yaginuma et al, , 2001. Apoptosis of cervical MNs is suppressed by transfection of the anti-apoptotic gene Bcl-2 (Sato et al, 2002b).…”

Section: Introductionmentioning

confidence: 99%

Motor neurons with limb-innervating character in the cervical spinal cord are sculpted by apoptosis based on the Hox code in chick embryo

et al. 2017

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In the developing chick embryo, a certain population of motor neurons (MNs) in the non-limb-innervating cervical spinal cord undergoes apoptosis between embryonic days 4 and 5. However, the characteristics of these apoptotic MNs remain undefined. Here, by examining the spatiotemporal profiles of apoptosis and MN subtype marker expression in normal or apoptosis-inhibited chick embryos, we found that this apoptotic population is distinguishable by Foxp1 expression. When apoptosis was inhibited, the Foxp1 MNs survived and showed characteristics of lateral motor column (LMC) neurons, which are of a limb-innervating subtype, suggesting that cervical Foxp1 MNs are the rostral continuation of the LMC. Knockdown and misexpression of Foxp1 did not affect apoptosis progression, but revealed the role of Foxp1 in conferring LMC identity on the cervical MNs. Furthermore, ectopic expression of Hox genes that are normally expressed in the brachial region prevented apoptosis, and directed Foxp1 MNs to LMC neurons at the cervical level. These results indicate that apoptosis in the cervical spinal cord plays a role in sculpting Foxp1 MNs committed to LMC neurons, depending on the Hox expression pattern.

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Distinct susceptibility of developing neurons to death following Bax overexpression in the chicken embryo

Cited by 7 publications

References 38 publications

Brn-3b enhances the pro-apoptotic effects of p53 but not its induction of cell cycle arrest by cooperating in trans-activation of bax expression

Brn-3b enhances the pro-apoptotic effects of p53 but not its induction of cell cycle arrest by cooperating in trans-activation of bax expression

Early neural cell death: numbers and cues from the developing neuroretina

Motor neurons with limb-innervating character in the cervical spinal cord are sculpted by apoptosis based on the Hox code in chick embryo

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