2011
DOI: 10.1242/dev.065193
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Abstract: SUMMARYThe well-known regulative properties of the sea urchin embryo, coupled with the recent elucidation of gene regulatory networks (GRNs) that underlie cell specification, make this a valuable experimental model for analyzing developmental plasticity. In the sea urchin, the primary mesenchyme cell (PMC) GRN controls the development of the embryonic skeleton. Remarkably, experimental manipulations reveal that this GRN can be activated in almost any cell of the embryo. Here, we focus on the activation of the … Show more

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Cited by 26 publications
(40 citation statements)
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“…Evidence of replacement was first seen about 3 hours after PMCs were removed from mesenchyme blastula stage embryos. At that time transcription factors specific for the skeletogenic fate were expressed by NSM indicating that reprogramming had been initiated (Ettensohn et al, 2007; Sharma and Ettensohn, 2011). These data suggested the possibility that reprogramming of the NSM was triggered quickly after cell loss.…”
Section: Resultsmentioning
confidence: 99%
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“…Evidence of replacement was first seen about 3 hours after PMCs were removed from mesenchyme blastula stage embryos. At that time transcription factors specific for the skeletogenic fate were expressed by NSM indicating that reprogramming had been initiated (Ettensohn et al, 2007; Sharma and Ettensohn, 2011). These data suggested the possibility that reprogramming of the NSM was triggered quickly after cell loss.…”
Section: Resultsmentioning
confidence: 99%
“…When skeletogenic cells were removed, either at the 16-cell stage as micromeres or at the mesenchyme blastula stage as PMCs, non-skeletogenic mesoderm cells (NSM) reprogrammed to assume a skeletogenic fate (Ettensohn and McClay, 1988; Sweet et al, 1999). If the PMCs and the archenteron tip (all mesoderm) were removed, the remaining presumptive endoderm reprogrammed to assume skeletal and other mesodermal fates (McClay and Logan, 1996; Sharma and Ettensohn, 2011). From these studies it was clear that the remaining mesoderm or even endoderm had the capacity to reprogram and replace missing skeletogenic cells.…”
Section: Introductionmentioning
confidence: 99%
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“…Activated Pmar1 in turn inhibits the transcriptional repressor HesC, resulting in derepression of the major skeletogenic TFs, including Alx1, Ets1 and Tbr Revilla-i-Domingo et al, 2007). The transcriptional activation of these skeletogenic TFs triggers specification of the large micromeres to become PMCs (Khaner and Wilt, 1991;Koga et al, 2010;Sharma and Ettensohn, 2010;Damle and Davidson, 2011;Sharma and Ettensohn, 2011;Lyons et al, 2014;Saunders and McClay, 2014). Alx1, which belongs to the evolutionarily conserved Cart1/Alx3/Alx4 family of Paired-class homeodomain proteins, plays a central role in the skeletogenesis of sea urchins and vertebrates (Ettensohn et al, 2003;Uz et al, 2010;Damle and Davidson, 2011;McGonnell et al, 2011;Dee et al, 2013).…”
Section: Introductionmentioning
confidence: 99%
“…Alx1, which belongs to the evolutionarily conserved Cart1/Alx3/Alx4 family of Paired-class homeodomain proteins, plays a central role in the skeletogenesis of sea urchins and vertebrates (Ettensohn et al, 2003;Uz et al, 2010;Damle and Davidson, 2011;McGonnell et al, 2011;Dee et al, 2013). Alx1 regulates the expression of other TFs and effector genes that are directly involved in spicule formation (biomineralization proteins) and genes involved in PMC motility and patterning (Snail, Twist, VegfR10) (Ettensohn et al, 2003;Sharma and Ettensohn, 2011;Rafiq et al, 2012). Knockdown (KD) of Alx1 in the sea urchin embryo results in decreased numbers of PMCs, delayed ingression of PMCs, failure to complete epithelial-to-mesenchymal transition (EMT) at mesenchyme blastula stage [24 h post fertilization (hpf )] due to the defects in de-adhesion, and a complete lack of skeletal rod formation (Ettensohn et al, 2003;Saunders and McClay, 2014).…”
Section: Introductionmentioning
confidence: 99%