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Mutation in the Drosophila melanogaster adenosine receptor gene selectively decreases the mosaic hyperplastic epithelial outgrowth rates in wts or dco heterozygous flies
- 1.0438115 - BC 2016 RIV NL eng J - Článek v odborném periodiku
Sidorov, Roman - Kučerová, Lucie - Kiss, I. - Žurovec, Michal
Mutation in the Drosophila melanogaster adenosine receptor gene selectively decreases the mosaic hyperplastic epithelial outgrowth rates in wts or dco heterozygous flies.
Purinergic Signalling. Roč. 11, č. 1 (2015), s. 95-105. ISSN 1573-9538. E-ISSN 1573-9546
Grant CEP: GA ČR GA14-27816S
GRANT EU: European Commission(CZ) FP7/2007-2013
Program: FP7
Institucionální podpora: RVO:60077344
Klíčová slova: cell competition * Adgf-A * Ent2
Kód oboru RIV: EB - Genetika a molekulární biologie
Impakt faktor: 3.196, rok: 2015
http://link.springer.com/article/10.1007%2Fs11302-014-9435-2
Adenosine (Ado) is a purine nucleoside that modulates many physiological processes in the body. It plays a prominent role as a paracrine signal of metabolic imbalance within tissues and serves as a signaling mechanism to coordinate tissue activity. Ado exerts a broad range of cytoprotective, growth-promoting, and immunosuppressive effects and was observed at a high concentration in a number of human tumors, it was therefore suggested to be an important factor regulating tumor growth. We developed a method for the measurement of the Ado effect on tumor growth in/Drosophila melanogaster/using the modification of somatic mutation and recombination test (SMART). In this report, we examined the effect of three/Drosophila/genes involved in Ado signaling on the incidence of somatic mosaic clones, including adenosine receptor (/AdoR/), adenosine transporter (/Ent2/), and adenosine deaminase/Adgf-A/. We show that genetic manipulations with these genes do not affect control clones, but cause dramatic changes in the frequency of hyperplastic clones established by the loss of heterozygosity (LOH) of the/warts/(/wts/) tumor suppressor gene/(wts/homolog in humans is called/LATS1/and its down-regulation has been reported in a number of tumors). The loss of/AdoR/function also decreases the frequency of/dco/tumor clones (human homolog of/dco/is called CK1δ). Our data show that adenosine and/warts/signaling pathways interact and adenosine signaling plays an important role in growth and survival of homozygous/wts^- /cells.
Trvalý link: http://hdl.handle.net/11104/0246737
Počet záznamů: 1