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During migration, crest cells destined for pharyngeal arches maintain contact with each other via [[lamellipodia]] and [[filopodia]]. Short range local contact is maintained with lamellipodia whilst long range non-local contact is maintained with filopodia.<ref name= "pmid15548586” > {{cite journal |vauthors= Teddy JM, Kulesa PM| title = In vivo evidence for short-and long-range cell communication in cranial neural crest cells | journal = Development,| volume = 131| issue=24 | pages =6141-6151| date = 2004| pmid = 15548586}}</ref> During this process, [[connexin 43]] (Cx43) regulates cell interaction by regulating the formation of channels known as [[gap junctions]].<ref name= “pmid17619792” > {{cite journal |vauthors= Snider P, Olaopa M, Firulli AB, Conway SJ | title = Cardiovascular development and the colonizing cardiac neural crest lineage| journal = The Scientific World Journal,| volume = 7 | pages = 1090-1113| date = 2007| pmid = 17619792}}</ref> Impaired Cx43 function in transgenic mice leads to altered coronary artery patterns and abnormal outflow tracts.<ref name= “pmid9640330” > {{cite journal |vauthors= Huang GY, Wessels A, Smith BR, Linask KK, Ewart JL, Lo CW| title = Alteration in connexin 43 gap junction gene dosage impairs conotruncal heart development | journal = Developmental biology,| volume = 198| pages = 32-44| date = 1998| pmid = 9640330}}</ref> Further gap junction signalling is dependent on a [[cadherin]] mediated cell adhesion formed during cross talking with p120 catenin signalling.<ref name= “pmid11449002” > {{cite journal |vauthors= Xu X, Li WE, Huang GY, Meyer R, Chen T, Luo Y, Thomas MP, Radice GL, Lo CW | title = Modulation of mouse neural crest cell motility by N-cadherin and connexin 43 gap junctions | journal = Journal of Cell Biology| volume = 154 | pages = 217-230| date = 2001| pmid= 11449002}}</ref>
Appropriate outflow tract formation relies on a [[morphogen]] concentration gradient set up by [[fibroblast growth factor]] (FGF) secreting cells. Cardiac crest cells furthest away from FGF secreting cells will receive lower concentrations of FGF8 signalling than cells closer to FGF secreting cells. This allows for appropriate formation of the outflow tract.<ref name= “pmid12223417” > {{cite journal |vauthors= Abu-Issa R, Smyth G, Smoak I, Yamamura K, Meyers EN | title = Fgf8 is required for pharyngeal arch and cardiovascular development in the mouse | journal = Development,| volume = 129| issue = 19 | pages = 4613-4625| date = 2002| pmid = 12223417}}</ref> Cells located in rhombomeres 3and 5 undergo programmed cell death under signalling cues from [[
The process of migration requires a permissive extracellular matrix.<ref name= “pmid20890117” >{{cite journal |vauthors= Kirby ML, Hutson MR | title = Factors controlling cardiac neural crest cell migration | journal = Cell adhesion & migration | volume = 4 | issue = 4 | pages = 609-621 | date = 2010 | pmid = 20890117| pmc = PMC3011257| doi = 10.4161/cam.4.4.13489}} </ref>. The [[enzyme]] [[arginyltransferase]] creates this environment by adding an arginyl group onto newly synthesised proteins during [[post-translational modification]].<ref name= “pmid20300656” > {{cite journal| vauthors= Kurosaka S, Leu NA, Zhang F, Bunte R, Saha S, Wang J, Guo C, He W, Kashina A| title = Arginylation-dependent neural crest cell migration is essential for mouse development. | journal = PLoS genetics,| volume = 6| issue =3 | pages = e1000878| date = 2010| pmid =20300656}}</ref> This process aids cells motility and ensures proteins the proteins contained within the actin cytoskeleton is prepped for migration.<ref name= “pmid20890117” >{{cite journal |vauthors= Kirby ML, Hutson MR | title = Factors controlling cardiac neural crest cell migration | journal = Cell adhesion & migration | volume = 4 | issue = 4 | pages = 609-621 | date = 2010 | pmid = 20890117| pmc = PMC3011257| doi = 10.4161/cam.4.4.13489}} </ref>
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