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Updated: Feb 18, 2026
Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
Published on: July 25, 2017
Selector genes display tumor cooperation and inhibition in Drosophila epithelium in a developmental context-dependent
Ram Prakash Gupta1, Anjali Bajpai1, Pradip Sinha2
1Department of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, India.
Abstract:
During animal development, selector genes determine identities of body segments and those of individual organs. Selector genes are also misexpressed in cancers, although their contributions to tumor progression per se remain poorly understood. Using a model of cooperative tumorigenesis, we show that gain of selector genes results in tumor cooperation, but in only select developmental domains of the wing, haltere and eye-antennal imaginal discs of Drosophila larva. Thus, the field selector, Eyeless (Ey), and the segment selector, Ultrabithorax (Ubx), readily cooperate to bring about neoplastic transformation of cells displaying somatic loss of the tumor suppressor, Lgl, but in only those developmental domains that express the homeo-box protein, Homothorax (Hth), and/or the Zinc-finger protein, Teashirt (Tsh). In non-Hth/Tsh-expressing domains of these imaginal discs, however, gain of Ey in lgl somatic clones induces neoplastic transformation in the distal wing disc and haltere, but not in the eye imaginal disc. Likewise, gain of Ubx in lgl somatic clones induces transformation in the eye imaginal disc but not in its endogenous domain, namely, the haltere imaginal disc. Our results reveal that selector genes could behave as tumor drivers or inhibitors depending on the tissue contexts of their gains.
Insights
Selector genes like Eyeless and Ultrabithorax can drive tumor growth in specific Drosophila tissues. Their oncogenic potential depends on the developmental context, acting as drivers or inhibitors in cancer progression.
Area of Science:
- Developmental Biology
- Cancer Biology
- Genetics
Background:
- Selector genes are crucial for establishing body segment and organ identities during development.
- Misexpression of selector genes is observed in cancers, but their precise role in tumor progression is unclear.
- Understanding selector gene function in cancer requires examining their context-dependent effects.
Purpose of the Study:
- To investigate how selector genes contribute to cooperative tumorigenesis in Drosophila.
- To determine the influence of tissue-specific expression patterns on selector gene-driven tumor formation.
- To elucidate the context-dependent roles of selector genes as tumor drivers or inhibitors.
Main Methods:
- Utilized a Drosophila model of cooperative tumorigenesis.
- Examined the effects of gain-of-function mutations in selector genes (Eyeless, Ultrabithorax) in combination with loss of the tumor suppressor Lgl.
- Analyzed tumor development within specific imaginal disc domains defined by expression of Homothorax and Teashirt.
Main Results:
- Gain of selector genes Eyeless (Ey) and Ultrabithorax (Ubx) promoted neoplastic transformation in specific Drosophila imaginal disc domains.
- Cooperation between Ey and Ubx in lgl mutant clones led to tumor formation, but only in domains expressing Homothorax (Hth) and/or Teashirt (Tsh).
- In non-Hth/Tsh domains, Ey induced transformation in the wing and haltere, while Ubx induced transformation in the eye disc, demonstrating context-specific effects.
Conclusions:
- Selector genes can act as tumor drivers or inhibitors depending on the developmental tissue context.
- The expression of other developmental regulators (Hth, Tsh) modulates the oncogenic potential of selector genes.
- These findings highlight the importance of tissue microenvironment in determining the role of developmental genes in cancer.
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