کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5532038 1401827 2016 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Transition between synaptic branch formation and synaptogenesis is regulated by the lin-4 microRNA
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیولوژی سلول
پیش نمایش صفحه اول مقاله
Transition between synaptic branch formation and synaptogenesis is regulated by the lin-4 microRNA
چکیده انگلیسی


• The lin-4 microRNA promotes synaptogenesis.
• The LIN-14 transcription factor inhibits synaptogenesis and promotes branch formation.
• LIN-14 promotes synaptic vesicle transport prior to branch formation.
• Genes implicated in synaptic vesicle transport are required for branch formation.

Axonal branch formation and synaptogenesis are sequential events that are required for the establishment of neuronal connectivity. However, little is known about how the transition between these two events is regulated. Here, we report that the lin-4 microRNA can regulate the transition between branch formation and synaptogenesis in the PLM axon of C. elegans. The PLM axon grows a collateral branch during the early L1 stage and undergoes synaptogenesis during the late L1 stage. Loss of the lin-4 microRNA disrupts synaptogenesis during the late L1 stage, suggesting that lin-4 promotes synaptogenesis. Conversely, the target of lin-4, the LIN-14 transcription factor, promotes PLM branch formation and inhibits synaptogenesis during the early L1 stage. Moreover, we present genetic evidence suggesting that synaptic vesicle transport is required for PLM branch formation and that the role of LIN-14 is to promote transport of synaptic vesicles to the region of future branch growth. These observations provide a novel mechanism whereby lin-4 promotes the transition from branch formation to synaptogenesis by repressing the branch-promoting and synaptogenesis-inhibiting activities of LIN-14.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Developmental Biology - Volume 420, Issue 1, 1 December 2016, Pages 60–66