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They showed it was possible to produce mature mouse sperm and use it to fertilise mouse eggs to produce viable offspring.

In a paper published online in the Proceedings of the National Academy of Sciences, they describe a simple way to signal immature mouse eggs to develop.

To measure whether the technique could diminish disease-causing mitochondrial mutations, the researchers created hybrid cells by fusing mouse eggs to human cells that harbor either of two disease-causing defects.

In 2004, Japanese researchers showed that they could alter imprinting genes in mouse eggs to create an artificial but fully parthenogenetic and viable baby.

We expressed MEK-EE, a constitutively activated form of MEK [36], [37], in mouse eggs to prevent the inactivation of MAPK that normally occurs several hours after egg activation.

In this study, we injected DNA beads into mouse eggs to induce spindle formation without kinetochores and studied the behavior of DNA beads after inducing anaphase of meiosis II.

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The minimal PLCζ concentration required for a physiologic pattern of Ca2+ oscillations was 0.0167 mg/mL, indicating that the amount of human PLCζ in mouse eggs able to induce Ca2+ oscillations and early embryogenesis was ∼80 fg/egg.

These enzymatic data indicate that both of these histidine mutations when introduced into human PLCζ dramatically diminish their PIP2 hydrolytic activity, thus directly explaining why the cRNA microinjection of these PLCζ mutants into unfertilized mouse eggs fails to induce normal egg activation.

He and colleagues developed a string of DNA that, when injected into the nucleus of a fertilized mouse egg, appears to make olfactory neurons more likely to develop one particular odorant receptor than the others.

The researchers injected nuclei from cumulus cells (a supporting cell that surrounds developing eggs) into intact mouse eggs, allowed each egg to rest for 2 to 3 hours, and then chemically induced cell division.

We and others showed previously that the cortex of mouse eggs is inductive to a general chromatin signal by inducing assembly of a distinct cortical structure, characterized by formation of a cortical actin cap [28], [29] enclosed by a myosin II ring (Deng et al., 2007).

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