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Mukherjee’s controversial piece on epigenetics #Drama

The scientific community is in uproar over Siddhartha Mukherjee’s latest piece for the New Yorker titled: Same but Different (you may know him from his novel Emperor of all maladies: a biography of cancer). His article highlights the study of epigenetics, and how recent findings may blur the line between nature and nurture. So why is the scientific community outraged? Vox explains:

 

Here’s the beef scientists have with Mukherjee and the New Yorker

The article is the type of piece the New Yorker usually is very good at: diving deep into a crevice of science and connecting it to veins of either history, politics, or the poetry of everyday life.

Mukherjee starts off with a personal tale. His mother and aunt are identical twins, and he muses on how their life experiences made them different people later on. He then connects this personal mystery with other mysteries in nature: Why are two ants genetically near identical but one is a worker and one is a boss?

In the story, what links these mysteries is the science of epigenetics, which, basically, explores how the environment can leave a lasting mark1 on how our genes work.

DNA is the instruction manual for life. So epigenetics may determine how likely those instructions are to be read. Understanding epigenetics is important because it could help us understand how we become more susceptible to disease (or not) over our lifetimes. And there’s some not-yet-conclusive evidence that epigenetic information is inheritable. As Vox’s Susannah Locke has explained, epigenetics means a person may pass on genes as well as experiences to a child.

But the article seems to have hit a nerve with some researchers who feel “epigenetics” has become a buzzword that’s distorting the science.

What Mukherjee (mainly) gets wrong, according to the scientists, is his explanation of how this process is thought to work. Mukherjee’s explanation is anchored in a discussion of histones, which are tiny proteins that act as a kind of a scaffolding for DNA. He leans heavily on the work of David Allis, a researcher at Rockefeller University, who has foundthese histones open and close specific sections of DNA, which he says changes the output of the genes.

“The coils of DNA seemed to open and close in response to histone modifications — inhaling, exhaling, inhaling, like life,” Mukherjee writes.

Next, Mukherjee notes (more vaguely) that scientists have found “other systems, too, that could scratch different kinds of code on the genome.”

There are two main points the scientists are clamoring over.

One is that they say Allis’s theory that histones actually change the output of genes is far from proven. In a second post on Coyne’s blog, Greally and Mark Ptashne, a biologist at Sloan Kettering, write, “there is no evidence that coiling and uncoiling of DNA has a causal effect on gene activity.”

The second is the critics say those glossed-over “other systems” are actually the prevailing theory on how it all works, and should be at least discussed at greater length.

The big, overarching, concept Mukherjee missed is “transcription factors,” which are proteins that can turn specific genes on and off. It’s these factors that scientists say should be the main focus of the explanation of how our genes are differentiated. And despite decades of research on them, transcription factors are hardly mentioned at all in the piece.

Steve Henikoff, a molecular biologist, writes on Coyne’s blog:

Mukherjee seemed not to realize that transcription factors occupy the top of the hierarchy of epigenetic information, that this has been widely accepted in the broader chromatin [i.e. DNA] field, and that histone modifications at most act as cogs in the machinery that enforces the often complex programs specified by the binding of transcription factors.

(To note: The scientists have other concerns with the piece. You can read more about those here.)

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