Ganglion mother cell

While each ganglion mother cell necessarily gives rise to two neurons, a neuroblast can asymmetrically divide multiple times.

[3][6] Research has suggested that certain tumor-suppressing proteins (Lgl, Dlg, or Brat) play a critical role in the asymmetric segregation of neural fate determinants and their localization to the basal cortex .

[6] In clonal lines of neuroblasts that had been manipulated so that they lacked Lgl activity, Miranda did not segregate asymmetrically, but was evenly distributed throughout the cortex.

The temporal regulation of neuroblast asymmetric division is controlled by proteins Hunchback (Hb) and sevenup (svp).

[1] Tumor formation occurs when TA-GMCs revert to type II neuroblasts resulting in a highly increased cellular proliferation.

[1] During the embryonic development of Drosophila, neuroblasts delaminate from their respective positions in the embryo and move towards the interior forming a ventral monolayer of cells, known as the neurogenic region.

The equivalent regions of neuronal growth in other common animal models do not have this symmetrical property, which makes Drosophila preferable for neurogenic study.

Each neuroblast can be traced through a lineage using methods such as green fluorescent protein transgene expression in order to investigate mechanisms of cellular diversity.

[2] Research has been conducted to observe the movement of neuroblasts and GMCs in the neurogenic region during embryonic development using molecular markers.

For instance the first five GMCs of NB7-1 (the neuroblast located in the 7th row and first column of the cortex) sequentially generate the U1-U5 motor neurons, and then subsequently 30 interneurons.

At the end of embryonic development neuroblasts become quiescent, but re-enter their cell cycles during later specific larval stages.

[3] An ortholog of Prospero in vertebrates (Prox1) is present in newly differentiating neurons and inhibits neural progenitor proliferation.

[3] Prospero is not present in the progeny of GMCs and is thought to act as a timer, promoting prospective neurons out of their cell cycle.

[5] Studying neurogenesis in animal models such as Drosophila comes with many advantages and leads to a better understanding of relevant human neurogenic analogs such as neural stem cells.

Type I neuroblast gives rise to a GMC and an identical neuroblast , as opposed to type II whose daughter cells are known as intermediate neural progenitors (INPs). The GMC then differentiates into two neurons. [ 1 ]
the signal protein Notch is exposed to both daughter cells of a neuroblast (another neuroblast and a GMC). Because Numb (represented by the blue line) is a Notch suppressor and only present in the GMC, the GMC will behave differently from the other daughter cell, the neuroblast.
Segregation of transcription factors during asymmetric division of a type I neuroblast
An example of a brain tumor occurring as a result of GMCs reverting to the neuroblast stage. Most likely caused by the absence of the Numb or Brat proteins in a type II neuroblast or possibly and absence of Prospero in a type I neuroblast
representation of neurogenesis in optic lobe development. During larval development the neuroepithelial cells(orange) transform into neuroblasts . NE cells undergo symmetric proliferation with a horizontal spindle orientation to expand the pool of precursor cells and give rise to asymmetrically dividing neuroblasts (green). Median neuroblasts divide asymmetrically with a vertical spindle orientation, localizing proteins i.e. Prospero. [ 9 ]