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Elucidating the Role of a Ubiquitin-Conjugating Enzyme Bendless during Drosophila Hematopoiesis
CC BY 4.0 · Indian J Med Paediatr Oncol 2024; 45(S 01): S1-S16
DOI: DOI: 10.1055/s-0044-1788214
*Corresponding author: (e-mail: rkhadilkar@actrec.gov.in).
Abstract
Background: Hematopoietic stem cell tissue homeostasis (HSCs) is governed by regulatory signals that maintain balance between self-renewal and differentiation via cell signaling networks like Hh, Wnt, and JAK/STAT signaling. The aim of our study is to elucidate the role of a ubiquitin-conjugating enzyme Bendless in Drosophila hematopoiesis.
Materials and Methods: In Drosophila, active hematopoiesis occurs in the Drosophila larval lymph gland (LG). We employ bendless loss of function mutants, UAS–Gal4 binary system to modulate Bendless gene expression in various cellular compartments of the lymph gland and then perform immunofluorescence-based analysis to study the regulation of hematopoiesis.
Results: Our results show that Bendless is expressed in various cellular subsets of the LG. Bendless loss of function mutants display abnormal hematopoiesis. Ben is also important in regulating niche size cell autonomously as well as nonautonomously. We show that zone-specific modulation of Bendless alters blood cell homeostasis in terms of niche size and differentiation either upon knockdown or overexpression of Bendless. Upon overexpressing Bendless in the hemocytes, we see upregulation of mRNA levels of JNK pathway targets Kayak, puckered and mmp1 and lamellocyte differentiation.
Conclusion: Our results indicate that Bendless regulates JNK targets and its over-expression leads to over-activation of the JNK pathway leading to lamellocyte differentiation. Bendless-mediated K63 ubiquitination could regulate multiple signaling pathways. Overall, based on our data, we speculate that both loss of Bendless or over-expression could be regulating different signaling pathways to control Drosophila hematopoiesis.
Publication History
Article published online:
08 July 2024
© 2024. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)
Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India
*Corresponding author: (e-mail: rkhadilkar@actrec.gov.in).
Abstract
Background: Hematopoietic stem cell tissue homeostasis (HSCs) is governed by regulatory signals that maintain balance between self-renewal and differentiation via cell signaling networks like Hh, Wnt, and JAK/STAT signaling. The aim of our study is to elucidate the role of a ubiquitin-conjugating enzyme Bendless in Drosophila hematopoiesis.
Materials and Methods: In Drosophila, active hematopoiesis occurs in the Drosophila larval lymph gland (LG). We employ bendless loss of function mutants, UAS–Gal4 binary system to modulate Bendless gene expression in various cellular compartments of the lymph gland and then perform immunofluorescence-based analysis to study the regulation of hematopoiesis.
Results: Our results show that Bendless is expressed in various cellular subsets of the LG. Bendless loss of function mutants display abnormal hematopoiesis. Ben is also important in regulating niche size cell autonomously as well as nonautonomously. We show that zone-specific modulation of Bendless alters blood cell homeostasis in terms of niche size and differentiation either upon knockdown or overexpression of Bendless. Upon overexpressing Bendless in the hemocytes, we see upregulation of mRNA levels of JNK pathway targets Kayak, puckered and mmp1 and lamellocyte differentiation.
Conclusion: Our results indicate that Bendless regulates JNK targets and its over-expression leads to over-activation of the JNK pathway leading to lamellocyte differentiation. Bendless-mediated K63 ubiquitination could regulate multiple signaling pathways. Overall, based on our data, we speculate that both loss of Bendless or over-expression could be regulating different signaling pathways to control Drosophila hematopoiesis.
No conflict of interest has been declared by the author(s).
Publication History
Article published online:
08 July 2024
© 2024. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)
Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India