|dc.description.abstract||Locomotion is essential for animals and it is regulated by crosstalk between neurons
and muscles. Although defects in the crosstalk between neurons and muscles are
implicated in many mobility related diseases in human, however, the underlying
molecular mechanisms have not been well characterized. In an attempt to gain
insights into the complex neuro-muscular crosstalk at molecular level, we have used
Drosophila melanogaster as model system to elucidate function of a gene, taxi,
mutations in the gene give rise to defective flight behavior resulting from a defective
The first chapter of this thesis explains how crosstalk between neurons and muscles
control different behaviors of Drosophila melanogaster, particularly locomotion.
Apart from locomotion, this chapter also explains how flies perform vision and how
they response to various stimuli. Second chapter explains materials and methods used
to complete the studies.
Third chapter explains genetic and phenotypic characterization of jumper mutant, an
allele of taxi gene. Further, based on experimental data, how the mutation affects the
taxi at both transcription and translational levels have been discussed. We found that
I-element insertion located at 5’UTR of the taxi in jumper is responsible for the
defective flight behavior in jumper mutant. The I-element insertion leads to increased
expression level of taxi in the head without affecting much of transcription and
translation in other body parts.
Fourth chapter explains the role of taxi in flight behavior of Drosophila melanogaster.
We found that knockdown of taxi in neurons gives rise to compromised flight ability.
Spatio-temporal conditional knockdown experiments suggest that taxi’s function is
critical at around 12 hours After Puparium Formation (APF). Further, from our RNA
sequencing result of taxi null, we found that the genes important for maintaining
membrane potential are differentially expressed. As a result, neuronal transmission
from brain to indirect flight muscles (IFMs) through peripherally synapsing
interneurons (PSI) gets altered, which might lead to reduction in wing beat duration of taxi mutants. We found that one of the main regulators of membrane potential is
Adar, a gene that is crucial to many molecular and physiological activities, and it is
repressed by taxi.
Fifth chapter of this thesis explains how taxi affects life span and phototaxis. We
found that over-expression of taxi in neurons beyond threshold shorten life span of
flies. It is also observed that phototaxis is abnormal with disruption in structure of
Six chapter of this thesis explains conclusion of the study.
Overall, in present study we have reported for the first time neuronal function of taxi in flight behavior, life span and phototransduction of Drosophila melanogaster.||en_US