The Division of Cells

The main purpose of this paper is to explain how the division of cells is highly regulated such that cells that fail to pass some specific stage-based tests cannot advance to the proceeding stages. Basically, the cycle is directly attached to some bioenergetic and biosynthetic demands, and prior to the division process, cell components in the parent cell have to be doubled and later distributed equally to the resulting daughter cells following a division process. This work hypothesizes that addition of phosphate moieties to the CDC25C by an enzyme called Adenosine Monophosphate-activated protein kinase acts as a mediator of a metabolic checkpoint that seeks to control cell division specifically at the point where the cells are transitioning from the G2 to the M phase. The research question that is being tested in this paper was about the activation of the protein kinase and how it works to be a high energy sensor that plays a significant role in cells that lack of the required bioenergy requirements that do not enter the mitotic phase during the cell division. The most important aspect of this experiment in the paper was about the HeLa cells which were subjected to chemicals that are known to activate the enzyme AMPK. Also, the main catabolic processes that are involved to generate energy for cells to transition from G1/G2 were determined by the application of radiochemical approaches, the experiment required to determine if AMPK activation had a hand in preventing mitosis. The results confirmed that activation of this enzyme prevented entry into mitosis. The paper presents a conflicting idea when it comes to the deciding if there is role of mTORC1 in the cell division process, so I think the weaknesses related to the experimental procedures that they designed, they activated AMPK or otherwise inactivated mTORC1 in a way that is not clearly proved and therefore following from this, one cannot really tell if the mitosis regulation was due to AMPK activation of mTORC1 inactivation. If this was my experiment, I would start with two separate setups should be conducted, one with activated AMPK and eliminated CDC25C to check whether there is any influence on mTORC1, and the other set up then will contain cells activated AMPK and have CDC25C and eliminated mTORC1. The results should then be cross-checked to see if AMPK only affects CDC25C or mTORC1 independently or both at the same time. This will help in the keen determination of the exact cause of cell cycle regulation when it comes to the cell division phases and stages.