Epigenetic cellular controls key for sperm and cancers

Sometimes in science there are unexpected threads tying seemingly very different things together.

Unraveling the knots in these threads can lead to new insights into important developmental processes and mechanisms of disease.

My lab studies epigenomic and transcription factors including a molecule called histone variant H3.3 (more here on H3.3).

H3.3 binds to the actual thread of DNA to create very different kinds of chromatin states than those made by the more traditional canonical histone H3 family members. Think of H3.3 as the unorthodox member of the histone H3 family.


Recent studies have indicated that H3.3 plays key roles in both stem cells and cancer.

The two genes that make H3.3 protein, H3f3a and H3f3b, are expressed differentially so cells may make their total pool of H3.3 protein only from the “a” gene or only the “b” gene or from both. We knocked out the “b” gene.

As a result, some genes switched inappropriately into “on” mode, while others that were supposed to be active were  switched off. The germ cell DNA was also not packaged properly. The end result was dead or dysfunctional sperm. In addition, earlier on in the spermatogenesis process, specific more primitive germ cell populations in the “b” knockouts died as well.

Read the full, original story: What do sperm have to do with brain tumors?

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