Saptaparna Pal, Amity University Kolkata
Some researchers from The Virginia School of Medicine have shed new light on how our brains mature; disclosing that the very last step in cell proliferation is important for the brain to reach its actual size and function. The new findings that are published in The Journal of Neuroscience identify a dedicated contributor to microcephaly, a birth defect in which the head is poorly developed and abnormally small. That’s because the head develops as the brain develops.
The Federal Centers for Disease Control confirms that microcephaly attacks 1 in 700 children to 1 in 5000 children in the United States each year. The condition is associated with developmental delays, learning disabilities, hearing and vision loss, movement impairment, and many other problems. By understanding the genetic cause behind microcephaly, even though they are rare, we can also help to understand how few viral infections cause microcephaly, such as cytomegalovirus or Zika Virus.
Dwyer and her team focus to understand how minute changes in individual cells can cause dramatic changes in the brain. In this case, they have identified a vital role for abscission, the concluding step in cell division. During abscission, a new or daughter cell splits its connection to its mother cell. Scientists have suspected that a cellular protein called Cep55 is crucial for proper abscission.
Neural stem cells in the prenatal brain appear to have tighter quality control than cells in the other parts of the body. If their DNA or organelles are damaged, they have a hair-trigger response to damage themselves, so that they don’t give rise to abnormal brain cells that might cause brain tumors or brain malfunction. Dwyer noted that blocking the cell death signal with gene therapy or drugs could help to reinstate brain growth in certain types of microcephaly, but it also can make brain function poor. Cep55 mutations also found associated with many human cancers, so understanding the normal function of Cep55 in proliferating cells in the brain helps inform cancer researchers how its altered function could lead to abnormal cell proliferation that can initiate or fuel tumor growth. Furthermore, NSCs that do stop abscission activate a signal for programmed cell death, whereas non-neural cells do not. Restricting this signal only partly reinstates brain growth showing that regulation of abscission is crucial for brain growth and development.
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Source: Little JN, McNeely KC, Michel N, Bott CJ, Lettieri KS, Hecht MR, Martin SA, Dwyer ND. Loss of Coiled-Coil Protein Cep55 Impairs Neural Stem Cell Abscission and Results in p53-Dependent Apoptosis in Developing Cortex. J Neurosci. doi: http://10.1523/JNEUROSCI.1955-20.2021.
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