Newt regeneration genes regulate Wingless signaling to restore patterning in Drosophila eye

被引:8
|
作者
Mehta, Abijeet Singh [1 ]
Deshpande, Prajakta [1 ]
Chimata, Anuradha Venkatakrishnan [1 ]
Tsonis, Panagiotis A. [1 ]
Singh, Amit [1 ,2 ,3 ,4 ,5 ]
机构
[1] Univ Dayton, Dept Biol, Dayton, OH 45469 USA
[2] Univ Dayton, Premed Program, Dayton, OH 45469 USA
[3] Univ Dayton, Ctr Tissue Regenerat & Engn Dayton TREND, Dayton, OH 45469 USA
[4] Univ Dayton, Integrat Sci & Engn Ctr, Dayton, OH 45469 USA
[5] Indiana State Univ, Ctr Genom Advocacy TCGA, Terre Haute, IN 47809 USA
关键词
SEGMENT POLARITY GENE; LIMB REGENERATION; CELL-DEATH; RETINAL DIFFERENTIATION; TRANSGENIC DROSOPHILA; MORPHOGENETIC FURROW; BOMBYX-MORI; EXPRESSION; APOPTOSIS; HEDGEHOG;
D O I
10.1016/j.isci.2021.103166
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Newts utilize their unique genes to restore missing parts by strategic regulation of conserved signaling pathways. Lack of genetic tools poses challenges to determine the function of such genes. Therefore, we used the Drosophila eye model to demonstrate the potential of 5 unique newt (Notophthalmus viridescens) gene(s), viropana1-viropana5 (vna1-vna5), which were ectopically expressed in L-2 mutant and GMR-hid, GMR-GAL4 eye. L-2 exhibits the loss of ventral half of early eye and head involution defective (hid) triggers cell-death during later eye development. Surprisingly, newt genes significantly restore missing photoreceptor cells both in L-2 and GMR>hid background by upregulating cell-proliferation and blocking cell death, regulating evolutionarily conserved Wingless (Wg)/Wnt signaling pathway and exhibit non-cell-autonomous rescues. Further, Wg/Wnt signaling acts downstream of newt genes. Our data highlights that unique newt proteins can regulate conserved pathways to trigger a robust restoration of missing photoreceptor cells in Drosophila eye model with weak restoration capability.
引用
收藏
页数:27
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