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The Role Of Isletl In Later Development Of Mouse Spinal Cord Motor Neurons

Posted on:2014-01-25Degree:MasterType:Thesis
Country:ChinaCandidate:M XinFull Text:PDF
GTID:2250330395491348Subject:Zoology
Abstract/Summary:PDF Full Text Request
The vertebrate nervous system is mainly composed of neurons and glial cells. Spinal motor neuron is very important class of neurons, which located in the ventral horn of the spinal cord. Motor neuron has a large size cell body, an axon and multiple dendrites. Motor neurons, which can directly or indirectly connect senior nerve and innervate muscle, conduct and receive signals, and then form the neural circuits to control motor behavior. Developmental defects and loss of function of motor neurons, will lead to a variety of motor neuron disease, such as Amyotrophic Lateral Sclerosis, spinal muscular atrophy.Previous studies have shown that transcription factor Isl1play a key role in the generation of spinal motor neurons, and knock out the Isl1cause motor neurons deletion. To further study the role of Isl1in the development of spinal motor neurons, we utilize the Cre/loxp system, with Hb9drive Cre to conditional knockout Isll in the spinal motor neurons. By detecting the expression of spinal MN-specific genes in different stages of Hb9-Cre;Isllloxp/loxp mutant mice, to study the role of transcription factor Isll in regulating MN continue development. The results showed that the mutants are significantly smaller than normal, and blood sugar levels rise markedly with a little movement defect in the behaviors, survived about two months until death.The absence of Isl1neither affect the survival of MN nor affect expression of other MN-specific genes, and the MN axonal projection from ventral horn also have no changes. The expression of Lhx3was enhanced, and the expression of Chx10expand more ventral spinal cord after Isl1deletion,Isl1still work on the boundaries of the V2interneuron and motor neuron domains.
Keywords/Search Tags:spinal motor neuron, conditional knockout, Is11, Hb9
PDF Full Text Request
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