The transcription factors AP-2β and AP-2α are required for survival of sympathetic progenitors and differentiated sympathetic neurons

Schmidt, Matthias; Huber, Leslie; Majdazari, Afsaneh; Schütz, Günther; Williams, Trevor; Rohrer, Hermann

doi:10.1016/j.ydbio.2011.04.011

Cited by 51 publications

(64 citation statements)

References 63 publications

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“…In mice the transcription factor TFAP2B is known to regulate noradrenaline signaling (Hong et al 2008;Schmidt et al 2011), and in Drosophila TFAP2B is encoded by the homolog TfAP-2 (Monge et al 2001). Since octopamine, the Drosophila analog of noradrenaline, is known to control aggression and mating behavior in males, we first wanted to determine if TfAP-2 was expressed in octopaminergic neurons.…”

Section: Tfap-2 Is Expressed In Octopaminergic Neuronsmentioning

confidence: 99%

“…TFAP2B is a member of the AP-2 family of transcription factors, key regulators of various developmental processes (Eckert et al 2005;Meng et al 2010;Wenke and Bosserhoff 2010), and in mice it was demonstrated that TFAP2B is necessary for the proper development of peripheral and central nervous system noradrenergic neurons (Hong et al 2008;Schmidt et al 2011). KCTD15 belongs to a family of potassium-channel tetramerization domain-containing proteins.…”

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confidence: 99%

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Regulation of Aggression by Obesity-Linked GenesTfAP-2andTwzThrough Octopamine Signaling inDrosophila

et al. 2014

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In Drosophila, the monoamine octopamine, through mechanisms that are not completely understood, regulates both aggression and mating behavior. Interestingly, our study demonstrates that the Drosophila obesity-linked homologs Transcription factor AP-2 (TfAP-2; TFAP2B in humans) and Tiwaz (Twz; KCTD15 in humans) interact to modify male behavior by controlling the expression of Tyramine b-hydroxylase and Vesicular monanime transporter, genes necessary for octopamine production and secretion. Furthermore, we reveal that octopamine in turn regulates aggression through the Drosophila cholecystokinin satiation hormone homolog Drosulfakinin (Dsk). Finally, we establish that TfAP-2 is expressed in octopaminergic neurons known to control aggressive behavior and that TfAP-2 requires functional Twz for its activity. We conclude that genetically manipulating the obesity-linked homologs TfAP-2 and Twz is sufficient to affect octopamine signaling, which in turn modulates Drosophila male behavior through the regulation of the satiation hormone Dsk.

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Section: Tfap-2 Is Expressed In Octopaminergic Neuronsmentioning

confidence: 99%

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confidence: 99%

Regulation of Aggression by Obesity-Linked GenesTfAP-2andTwzThrough Octopamine Signaling inDrosophila

et al. 2014

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“…However, it has not yet been possible to examine the consequence of removing all three Tfap2 paralogs in melanocytes due to another example of redundancy, the lack of neural crest in zebrafish depleted of both Tfap2a and Tfap2c [33,34]. This is also true in mouse, where Tfap2a and Tfap2b are expressed in early neural crest [35] as well as the melanocyte lineage, resulting in almost complete loss of migrating trunk neural crest prior to specification of the melanocyte lineage in Tfap2a/Tfap2b double mutants [36]. Thus, the specific contributions of these factors to the GRN governing melanocyte differentiation have not been thoroughly evaluated.…”

Section: Introductionmentioning

confidence: 99%

TFAP2 paralogs regulate melanocyte differentiation in parallel with MITF

et al. 2017

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Mutations in the gene encoding transcription factor TFAP2A result in pigmentation anomalies in model organisms and premature hair graying in humans. However, the pleiotropic functions of TFAP2A and its redundantly-acting paralogs have made the precise contribution of TFAP2-type activity to melanocyte differentiation unclear. Defining this contribution may help to explain why TFAP2A expression is reduced in advanced-stage melanoma compared to benign nevi. To identify genes with TFAP2A-dependent expression in melanocytes, we profile zebrafish tissue and mouse melanocytes deficient in Tfap2a, and find that expression of a small subset of genes underlying pigmentation phenotypes is TFAP2A-dependent, including Dct, Mc1r, Mlph, and Pmel. We then conduct TFAP2A ChIP-seq in mouse and human melanocytes and find that a much larger subset of pigmentation genes is associated with active regulatory elements bound by TFAP2A. These elements are also frequently bound by MITF, which is considered the “master regulator” of melanocyte development. For example, the promoter of TRPM1 is bound by both TFAP2A and MITF, and we show that the activity of a minimal TRPM1 promoter is lost upon deletion of the TFAP2A binding sites. However, the expression of Trpm1 is not TFAP2A-dependent, implying that additional TFAP2 paralogs function redundantly to drive melanocyte differentiation, which is consistent with previous results from zebrafish. Paralogs Tfap2a and Tfap2b are both expressed in mouse melanocytes, and we show that mouse embryos with Wnt1-Cre-mediated deletion of Tfap2a and Tfap2b in the neural crest almost completely lack melanocytes but retain neural crest-derived sensory ganglia. These results suggest that TFAP2 paralogs, like MITF, are also necessary for induction of the melanocyte lineage. Finally, we observe a genetic interaction between tfap2a and mitfa in zebrafish, but find that artificially elevating expression of tfap2a does not increase levels of melanin in mitfa hypomorphic or loss-of-function mutants. Collectively, these results show that TFAP2 paralogs, operating alongside lineage-specific transcription factors such as MITF, directly regulate effectors of terminal differentiation in melanocytes. In addition, they suggest that TFAP2A activity, like MITF activity, has the potential to modulate the phenotype of melanoma cells.

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“…Among the AP2 factors, AP2α, AP2β and AP2γ are reported to be the key regulators in neural crest development [25][26][27][28], which is generally thought to occur following the neural plate formation. Conditional disruption of Smad4 in neural crest cells results in AP2α downregulation from embryonic day 9.5 (E9.5) in mouse embryo [29].…”

Section: Introductionmentioning

confidence: 99%

AP2γ regulates neural and epidermal development downstream of the BMP pathway at early stages of ectodermal patterning

et al. 2012

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Bone morphogenetic protein (BMP) inhibits neural specification and induces epidermal differentiation during ectodermal patterning. However, the mechanism of this process is not well understood. Here we show that AP2γ, a transcription factor activator protein (AP)-2 family member, is upregulated by BMP4 during neural differentiation of pluripotent stem cells. Knockdown of AP2γ facilitates mouse embryonic stem cell (ESC) neural fate determination and impairs epidermal differentiation, whereas AP2γ overexpression inhibits neural conversion and promotes epidermal commitment. In the early chick embryo, AP2γ is expressed in the entire epiblast before HH stage 3 and gradually shifts to the putative epidermal ectoderm during HH stage 4. In the future neural plate AP2γ inhibits excessive neural expansion and it also promotes epidermal development in the surface ectoderm. Moreover, AP2γ knockdown in ESCs and chick embryos partially rescued the neural inhibition and epidermal induction effects of BMP4. Mechanistic studies showed that BMP4 directly regulates AP2γ expression through Smad1 binding to the AP2γ promoter. Taken together, we propose that during the early stages of ectodermal patterning in the chick embryo, AP2γ acts downstream of the BMP pathway to restrict precocious neural expansion in the prospective neural plate and initiates epidermal differentiation in the future epidermal ectoderm.

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The transcription factors AP-2β and AP-2α are required for survival of sympathetic progenitors and differentiated sympathetic neurons

Cited by 51 publications

References 63 publications

Regulation of Aggression by Obesity-Linked GenesTfAP-2andTwzThrough Octopamine Signaling inDrosophila

Regulation of Aggression by Obesity-Linked GenesTfAP-2andTwzThrough Octopamine Signaling inDrosophila

TFAP2 paralogs regulate melanocyte differentiation in parallel with MITF

AP2γ regulates neural and epidermal development downstream of the BMP pathway at early stages of ectodermal patterning

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