Tubulin-binding cofactor E-like (TBCEL), the protein product of the mulet gene, is required in the germline for the regulation of inter-flagellar microtubule dynamics during spermatid individualization
| Autor: | Nicole DeSouza, Janet Rollins, Christopher Bazinet, Matthew Vicioso, Danielle Quaranto, Vincent Lombardo, Gabriela Mendoza, Elissa Innabi, Dwaine Pryce, Rachel Daniel, Stephanie Wegener, Marielle Villanobos, Kavita Bharrat, Erin Dailey, Victoria Siracusa, James J. Fabrizio, Simon Innabi, Vrutant Patel, Iryna Koziy, Amir Niknejad, Stephanie Rodway, Elisa Ferrara, Justin Pronovost |
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| Rok vydání: | 2020 |
| Předmět: |
Male
0106 biological sciences QH301-705.5 Spermiogenesis Science Population Mutant Fluorescent Antibody Technique Biology 01 natural sciences General Biochemistry Genetics and Molecular Biology Germline Tubulin binding 03 medical and health sciences Microtubule Testis medicine Animals Drosophila Proteins Biology (General) education 030304 developmental biology 0303 health sciences education.field_of_study Spermatid Wild type Spermatids mulet spermatogenesis 3. Good health Cell biology Germ Cells Phenotype medicine.anatomical_structure Gene Expression Regulation tbce-like individualization Gene Knockdown Techniques Mutation Drosophila General Agricultural and Biological Sciences Research Article Molecular Chaperones 010606 plant biology & botany |
| Zdroj: | Biology Open, Vol 9, Iss 2 (2020) Biology Open |
| ISSN: | 2046-6390 |
| Popis: | Individual sperm cells are resolved from a syncytium during late step of spermiogenesis known as individualization, which is accomplished by an Individualization Complex (IC) composed of 64 investment cones. mulet encodes Tubulin-binding cofactor E-like (TBCEL), suggesting a role for microtubule dynamics in individualization. Indeed, a population of ∼100 cytoplasmic microtubules fails to disappear in mulet mutant testes during spermatogenesis. This persistence, detected using epi-fluorescence and electron microscopy, suggests that removal of these microtubules by TBCEL is a prerequisite for individualization. Immunofluorescence reveals TBCEL expression in elongated spermatid cysts. In addition, testes from mulet mutant males were rescued to wild type using tubulin-Gal4 to drive TBCEL expression, indicating that the mutant phenotype is caused by the lack of TBCEL. Finally, RNAi driven by bam-GAL4 successfully phenocopied mulet, confirming that mulet is required in the germline for individualization. We propose a model in which the cytoplasmic microtubules serve as alternate tracks for investment cones in mulet mutant testes. This article has an associated First Person interview with the first author of the paper. Summary: The leading cause of human male infertility is a failure to resolve spermatids from a germline syncytium during spermatid individualization. Here we characterize a mutation that disrupts this process. |
| Databáze: | OpenAIRE |
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