Hypothesis 1: pMN progenitor fate is biased by the position of the cell within the pMN domain.
Experimental Approach: Transgenic olig2:EGFP;actb2:mCherry donor embryos cells were transplanted into stage-matched wild-type hosts. Confocal time-lapse microscopy was used to image individual EGFP+ mCherry+ pMN cells continuously until 42 hpf, assess the behaviors
of individual progenitors within the pMN domain. Division of the cells was …show more content…
pMN progenitors moved radially from the spinal cord lumen to differentiate into motor neurons. Decision for progenitor to differentiate to a neuron or to divide depends on its position on the dorsoventral axis.
Concern (if any): Why the pMN progenitor pool is not maintained by self-renewing divisions? What happens if these progenitors are damaged or are mutated?
Hypothesis 2: Distinct cell lineages give rise to motor neurons and glial cells that affect the timing of olig2 expression initiation.
Experimental Approach: To determine the timing of the olig2 initiation, UV light convertible Kaede-fluorescent protein was utilized. A color change from green to red would indicate an expression of olig2. Embryos were photoconverted 24 hpf and were analyzed at 72 hpf.
Major Findings: Dorsolaterally migrated motor neurons were red, while dorsally migrated oligodendrocyte precursor cells were green. Timing of olig2 initiation between the two cells further supports the heterogenous model. In addition to difference in timing, ventral spinal cord cells slowly gain pMN identity.