Nonsense-mediated mRNA decay (NMD) is a surveillance pathway that cleans the system from possible harmful proteins and also regulates up to 10% of normal RNAs. The essential player proteins in the NMD (core NMD factors) are Upf1, Upf2, and Upf3. Mutation of any of these NMD factors cause ranges of effects in the development of various organisms. In humans, mutation of Upf3 was associated with neurodegenerative disorders, which include: attention deficit, schizophrenia autism, and intellectual disability. Using functional genetics approach and behavioral analysis methods we examined the loss of function effects of Upf3, in the nervous system function of a Drosophila melanogaster. We observed certain nervous system functional defects in homozygous Upf3 mutants. The embryos exhibited reduced and delayed hatching, the larvae manifested defects in motor function and the adults showed reduced climbing ability, defective short term memory, and learning, and notably, the adult life span was also reduced. This work has further revealed the prospect of Upf3 as a player gene for consideration in the management of neurodegenerative diseases. We explored this using Drosophila melanogaster as a model organism to mimic and study the neurodegenerative traits observed in the patients suffering from Upf3 mutation. Likewise, it suggests a further investigation into the mechanistic insight for the roles of Upf3 in both early and late CNS development.
Published in | Advances in Biochemistry (Volume 8, Issue 2) |
DOI | 10.11648/j.ab.20200802.12 |
Page(s) | 38-44 |
Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
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Copyright © The Author(s), 2020. Published by Science Publishing Group |
Nonsense-mediated mRNA Decay, NMD Factors, Organismal Development, Neurodegenerative Behaviors, Drosophila melanogaster
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APA Style
Sanusi Ahmed Jega, Ahmed Adebowole Adedeji, Marta Vicente-Crespo. (2020). Manifestation of Functional Defects of Nervous System in Upf3 Mutants Drosophila melanogaster at Larval and Adult Stages. Advances in Biochemistry, 8(2), 38-44. https://doi.org/10.11648/j.ab.20200802.12
ACS Style
Sanusi Ahmed Jega; Ahmed Adebowole Adedeji; Marta Vicente-Crespo. Manifestation of Functional Defects of Nervous System in Upf3 Mutants Drosophila melanogaster at Larval and Adult Stages. Adv. Biochem. 2020, 8(2), 38-44. doi: 10.11648/j.ab.20200802.12
AMA Style
Sanusi Ahmed Jega, Ahmed Adebowole Adedeji, Marta Vicente-Crespo. Manifestation of Functional Defects of Nervous System in Upf3 Mutants Drosophila melanogaster at Larval and Adult Stages. Adv Biochem. 2020;8(2):38-44. doi: 10.11648/j.ab.20200802.12
@article{10.11648/j.ab.20200802.12, author = {Sanusi Ahmed Jega and Ahmed Adebowole Adedeji and Marta Vicente-Crespo}, title = {Manifestation of Functional Defects of Nervous System in Upf3 Mutants Drosophila melanogaster at Larval and Adult Stages}, journal = {Advances in Biochemistry}, volume = {8}, number = {2}, pages = {38-44}, doi = {10.11648/j.ab.20200802.12}, url = {https://doi.org/10.11648/j.ab.20200802.12}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ab.20200802.12}, abstract = {Nonsense-mediated mRNA decay (NMD) is a surveillance pathway that cleans the system from possible harmful proteins and also regulates up to 10% of normal RNAs. The essential player proteins in the NMD (core NMD factors) are Upf1, Upf2, and Upf3. Mutation of any of these NMD factors cause ranges of effects in the development of various organisms. In humans, mutation of Upf3 was associated with neurodegenerative disorders, which include: attention deficit, schizophrenia autism, and intellectual disability. Using functional genetics approach and behavioral analysis methods we examined the loss of function effects of Upf3, in the nervous system function of a Drosophila melanogaster. We observed certain nervous system functional defects in homozygous Upf3 mutants. The embryos exhibited reduced and delayed hatching, the larvae manifested defects in motor function and the adults showed reduced climbing ability, defective short term memory, and learning, and notably, the adult life span was also reduced. This work has further revealed the prospect of Upf3 as a player gene for consideration in the management of neurodegenerative diseases. We explored this using Drosophila melanogaster as a model organism to mimic and study the neurodegenerative traits observed in the patients suffering from Upf3 mutation. Likewise, it suggests a further investigation into the mechanistic insight for the roles of Upf3 in both early and late CNS development.}, year = {2020} }
TY - JOUR T1 - Manifestation of Functional Defects of Nervous System in Upf3 Mutants Drosophila melanogaster at Larval and Adult Stages AU - Sanusi Ahmed Jega AU - Ahmed Adebowole Adedeji AU - Marta Vicente-Crespo Y1 - 2020/05/14 PY - 2020 N1 - https://doi.org/10.11648/j.ab.20200802.12 DO - 10.11648/j.ab.20200802.12 T2 - Advances in Biochemistry JF - Advances in Biochemistry JO - Advances in Biochemistry SP - 38 EP - 44 PB - Science Publishing Group SN - 2329-0862 UR - https://doi.org/10.11648/j.ab.20200802.12 AB - Nonsense-mediated mRNA decay (NMD) is a surveillance pathway that cleans the system from possible harmful proteins and also regulates up to 10% of normal RNAs. The essential player proteins in the NMD (core NMD factors) are Upf1, Upf2, and Upf3. Mutation of any of these NMD factors cause ranges of effects in the development of various organisms. In humans, mutation of Upf3 was associated with neurodegenerative disorders, which include: attention deficit, schizophrenia autism, and intellectual disability. Using functional genetics approach and behavioral analysis methods we examined the loss of function effects of Upf3, in the nervous system function of a Drosophila melanogaster. We observed certain nervous system functional defects in homozygous Upf3 mutants. The embryos exhibited reduced and delayed hatching, the larvae manifested defects in motor function and the adults showed reduced climbing ability, defective short term memory, and learning, and notably, the adult life span was also reduced. This work has further revealed the prospect of Upf3 as a player gene for consideration in the management of neurodegenerative diseases. We explored this using Drosophila melanogaster as a model organism to mimic and study the neurodegenerative traits observed in the patients suffering from Upf3 mutation. Likewise, it suggests a further investigation into the mechanistic insight for the roles of Upf3 in both early and late CNS development. VL - 8 IS - 2 ER -