Review Mechanism for Complexity in Brain The study on the review mechanism for the complexity of the brain as put forth by Boyan and Reichert is a research which was conducted with the aim of showing that the cells comprising the complex circuitry of the central complex development of Drosophila and grasshopper are surprisingly generated by small number of primary progenitor. The question raised here is whether this complex circuitry is truly generated by this small number of primary progenitor. The study hypothesizes that a general mechanism for generating complexity in a young brain of both insects and mammals is by amplification of neuron proliferation through self-renewing cells of intermediate progenitor (Boyan & Reichert, 2011). It has been found that some of the neurons from the mammalian brain originate from directly from the NSC division while many other neurons including the glial cells, well pronounced in the growing mammalian cortex, are indirectly generated by NSC through one or multiple rounds of divisions of the INPs. This is also known as basal progenitors which has more restricted potential. Therefore, in the mammalian cortical development, similar to the insect central complex development, the progenitor cells which are intermediate and analogous in function to the transit amplifying cells found in the stem cell lineages in varied tissues, play a pool function in the amplification of proliferation needed to generate the numerous number of neuron cells required to make up complex neural circuitry. Due to our glitch of the self-renewing INP cells, cells have only been reported to be in insects and mammals. This brings clearly the platform for the next study to determine whether the INP dependent amplification of NSC proliferation could be having a possibility of happening in other different animal taxa and consequently if this is the general way of increasing the size and also complexity of the brain during development and evolution. The amplification of NSC has been documented to be prone to proliferative deregulations and results show that it can lead to tumor formation in a case where genes involved in asymmetric cell fate determination become defective whereas the amplification of NSC proliferation though INPs is available in type II lineages contribute to the enormous number of neurons needed for central complex development. The mutational analysis of the development of the Drosophila brain shows clearly that the malfunctioning of the mechanisms that control the proliferative branches of NSCs or the developmental fate of the daughter cells progenitors is again one of the principle major causes of malignant transformation of the cells. So many genetic studies focused asymmetric segregation of cell-fate determinants in NSCs have opened the tumor suppressor activity of such determinants. Major determinants among others are the cell-fate determinants Prospero, brat and Numb in The mutational loss of function of any of the three outcomes in dramatic primary brain tumors in drosophila. Transplantation of the corresponding mutant brain tissues into just normal host flies comes up with lethal malignant tumors and brings about the formation of metastasis and the tumors coming from this can then successively be re-implanted into new host for several years. Giving it another view of rate of growth, cell type and metastatic activity, the tumors that are induced by the transplant are essentially indistinguishable from one tumor to the other. This supports the known assumption that all the tumors might have a common etiology which is the perturbation of cell determinants in NSCs. Several evidential lines show that type II NSC lineages an example being those that normally contribute neural progeny to central complex development, are major contributors to the brain tumors , the types which are induced by dysregulation of cell fate determinants. The study informs us that analysis of the tumor phenotypes shows that the cells that are overgrowing most regularly arise in a specific location in the dorsal part of the brain hemispheres and in this same region is where we find the amplifying type II lineages. Secondly, the disability in function of brat and numb specifically in type II NSC, brings about unspecified INPs that in the contrary are not able to produce differentiated neural progeny and starts tumorigenic overgrowth. The molecular genetics transformation of the amplifying type II NSCs, in the third position, to non-amplifying type I NSCs, seems to abolish the tumorigenic phenotype, at least if not in all, but just in brat mutants. Therefore the neural progenitors in the insects brain involved in a type of independent amplifying mode of neurogenesis as compared to that seen in the mammalian brain also comes out to be the most prone tumorigenic (Young & Armstrong, 2010). Work cited Boyan, G., & Reichert, H. (2011). Trends in Neuroscience. Mechanisms for Complexity in Brain , pp247-257. Young, J., & Armstrong, J. (2010). Building the Central Complex. The generation and Development District Subset , PP1525-1541.