Cellular Biology Wiz Needed 1) Bonus Cytoplasm from a mitotic cell is injected i

Question

Cellular Biology Wiz Needed

1) Bonus Cytoplasm from a mitotic cell is injected into a call cell A) stuck in G2. This causes the cell A to enter M. phase. A sample of the injected cell A cytoplasm is injected into another G2 cell cell B) Cell B enters M phase This can be repeated many times until none of the protein from the original cell remains, and subsequently injected G2 cells still enter M phase in perpetuity. What is an explanation for this observation? (2.5 points) 2) HER2 is overexpressed through gene amplification in HER2+ breast cancers. The wild-type HER2 is made (it's sequence isn't changed), but there is much more protein than normal. Normally, HER2 dimerizes with growth factor bound RTKS, which leads to its activation. However, in HER2 amplified breast cancers, HER2 dimerizes with itself and activates itself independently of growth factor binding. Why would HER2 overexpression enable this dimerization and activation without a ligand? (2.5 points)

Explanation / Answer

1) The G2/M checkpoint prevents the cell from entering mitosis phase M. Increased amounts of cyclin B/CDK1 (cyclin dependent kinase 1) are required for the cell to enter M phase. A cell stuck in G2 phase has less levels of cyclin B and CDK1. Cyclin B/CDK1 is known as the M phase promoting factor or MPF. It is present in high amounts in cytoplasm of mitotic cell. Hence, if cytoplasm is injected in a G2 arrested cell, the levels of MPF or Cyclin B/CDK1 increase allowing the G2 arrested cell to enter M phase.

2) HER2 is the only human epidermal growth factor receptor isoform that is capable of ligand independent activation. There is no existing ligand known that can promoter HER2-HER2 homo dimer formation, although heterodimers formation can occur in response to ligands.

HER2 dimerization occurs due to interactions between domain II(B) of HER2 and domains I(A) and III(A) of another HER2. The extracellular domain of HER2 plays an essential role in ErbB2 dimerization. Two Her2 protomers directly bind to each other when there is interaction between the dimerization arm and the C-shaped pocket. HER2 can form signaling active homodimers only when it is in a constitutively active configuration. Such configurations are absent when the levels of HER2 are at physiological normal levels. Only when HER2 levels are increased due to overexpression will HER2 have a spontaneous and constitutive active configuration. 96–998 in the C-terminal tail of HER2 is required for HER2 to form homodimers. When the gene is overexpressed, this C-terminal domain becomes constitutively active, resulting in homodimer formation. This also cause the Upregulation of its kinase activity.

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