scholarly journals Temporal identity establishes columnar neuron morphology, connectivity, and function in a Drosophila navigation circuit

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Luis F Sullivan ◽  
Timothy L Warren ◽  
Chris Q Doe

The insect central complex (CX) is a conserved brain region containing 60 + neuronal subtypes, several of which contribute to navigation. It is not known how CX neuronal diversity is generated or how developmental origin of subtypes relates to function. We mapped the developmental origin of four key CX subtypes and found that neurons with similar origin have similar axon/dendrite targeting. Moreover, we found that the temporal transcription factor (TTF) Eyeless/Pax6 regulates the development of two recurrently-connected CX subtypes: Eyeless loss simultaneously produces ectopic P-EN neurons with normal axon/dendrite projections, and reduces the number of E-PG neurons. Furthermore, transient loss of Eyeless during development impairs adult flies’ capacity to perform celestial navigation. We conclude that neurons with similar developmental origin have similar connectivity, that Eyeless maintains equal E-PG and P-EN neuron number, and that Eyeless is required for the development of circuits that control adult navigation.

2018 ◽  
Author(s):  
Luis F. Sullivan ◽  
Timothy L. Warren ◽  
Chris Q. Doe

AbstractThe insect central complex (CX) is a conserved brain region containing 60+ neuronal subtypes, several of which contribute to navigation. It is not known how CX neuronal diversity is generated or how developmental origin of subtypes relates to function. We mapped the developmental origin of four key CX subtypes and found that neurons with similar origin have matching axon/dendrite targeting. Moreover, we found that the temporal transcription factor (TTF) Eyeless/Pax6 regulates the development of two recurrently-connected CX subtypes: Eyeless loss simultaneously produces ectopic P-EN neurons with normal axon/dendrite projections, and reduces the number of E-PG neurons. Furthermore, the transient loss of Eyeless during development impairs adult flies’ capacity to perform celestial navigation. We conclude that neurons with similar developmental origin have similar connectivity, that Eyeless maintains equal E-PG and P-EN neuron number, and that Eyeless is required for the development of circuits that control adult navigation.


Cell Reports ◽  
2021 ◽  
Vol 36 (4) ◽  
pp. 109446
Author(s):  
Benjamin Bourgeois ◽  
Tianshu Gui ◽  
Diana Hoogeboom ◽  
Henry G. Hocking ◽  
Gesa Richter ◽  
...  

2014 ◽  
Vol 206 (4) ◽  
pp. 1364-1377 ◽  
Author(s):  
Marçal Soler ◽  
Eduardo Leal Oliveira Camargo ◽  
Victor Carocha ◽  
Hua Cassan-Wang ◽  
Hélène San Clemente ◽  
...  

2017 ◽  
Vol 53 ◽  
pp. S92
Author(s):  
Miroslava Kardosova ◽  
Lucie Potuckova ◽  
Ivana Halova ◽  
Polina Zjablovskaja ◽  
Lubica Draberova ◽  
...  

2019 ◽  
Vol 5 (8) ◽  
pp. eaaw0480 ◽  
Author(s):  
Theodore T. Drashansky ◽  
Eric Helm ◽  
Zhiguang Huo ◽  
Nina Curkovic ◽  
Preet Kumar ◽  
...  

Regulatory T (Treg) cells are essential for peripheral tolerance and rely on the transcription factor (TF) Foxp3 for their generation and function. Several other TFs are critical for the Treg cell program. We found that mice deficient in Bcl11b TF solely in Treg cells developed fatal autoimmunity, and Bcl11b-deficient Treg cells had severely altered function. Bcl11b KO Treg cells showed decreased functional marker levels in homeostatic conditions, inflammation, and tumors. Bcl11b controlled expression of essential Treg program genes at steady state and in inflammation. Bcl11b bound to genomic regulatory regions of Treg program genes in both human and mouse Treg cells, overlapping with Foxp3 binding; these genes showed altered chromatin accessibility in the absence of Bcl11b. Additionally, Bcl11b restrained myeloid and NK cell programs in Treg cells. Our study provides new mechanistic insights on the Treg cell program and identity control, with major implications for therapies in autoimmunity and cancer.


2019 ◽  
Author(s):  
Austin Q. Seroka ◽  
Chris Q. Doe

AbstractThe generation of neuronal diversity is essential for circuit formation and behavior. Morphological differences in sequentially born neurons could be due to intrinsic molecular identity specified by temporal transcription factors (henceforth called intrinsic temporal identity) or due to changing extrinsic cues. Here we use the Drosophila NB7-1 lineage to address this question. NB7-1 sequentially generates the U1-U5 motor neurons; each has a distinct intrinsic temporal identity due to inheritance of a different temporal transcription factor at time of birth. Here we show that the U1-U5 neurons project axons sequentially, followed by sequential dendrite extension. We misexpress the earliest temporal transcription factor, Hunchback, to create “ectopic” U1 neurons with an early intrinsic temporal identity but later birth-order. These ectopic U1 neurons have axon muscle targeting and dendrite neuropil targeting consistent with U1 intrinsic temporal identity, rather than their time of birth or differentiation. We conclude that intrinsic temporal identity plays a major role in establishing both motor axon muscle targeting and dendritic arbor targeting, which are required for proper motor circuit development.


2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Ganesh Vinayak Samant ◽  
Kallal Pramanik ◽  
Noah Leigh ◽  
Mark Horswill ◽  
Monica Beltrame ◽  
...  

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