What is epigenetics Carlos GuerreroBosagna

Here’s a conundrum:

identical twins originate
from the same DNA,

so how can they turn out so different

even in traits that have a significant
genetic component?

For instance, why might one twin
get heart disease at 55,

while her sister runs marathons
in perfect health?

Nature versus nurture
has a lot to do with it,

but a deeper related answer can be found
within something called epigenetics.

That’s the study of how DNA interacts

with the multitude of smaller molecules
found within cells,

which can activate and deactivate genes.

If you think of DNA as a recipe book,

those molecules are largely what determine
what gets cooked when.

They aren’t making any conscious
choices themselves,

rather their presence and concentration
within cells makes the difference.

So how does that work?

Genes in DNA are expressed when they’re
read and transcribed into RNA,

which is translated into proteins
by structures called ribosomes.

And proteins are much of what determines
a cell’s characteristics and function.

Epigenetic changes can boost or interfere
with the transcription of specific genes.

The most common way interference happens
is that DNA,

or the proteins it’s wrapped around,

gets labeled with small chemical tags.

The set of all of the chemical tags
that are attached to the genome

of a given cell

is called the epigenome.

Some of these, like a methyl group,
inhibit gene expression

by derailing the cellular
transcription machinery

or causing the DNA to coil more tightly,

making it inaccessible.

The gene is still there, but it’s silent.

Boosting transcription is essentially
the opposite.

Some chemical tags will unwind the DNA,
making it easier to transcribe,

which ramps up production
of the associated protein.

Epigenetic changes can survive
cell division,

which means they could affect
an organism for its entire life.

Sometimes that’s a good thing.

Epigenetic changes are part
of normal development.

The cells in an embryo start
with one master genome.

As the cells divide,
some genes are activated

and others inhibited.

Over time, through this epigenetic
reprogramming,

some cells develop into heart cells,

and others into liver cells.

Each of the approximately 200
cell types in your body

has essentially the same genome

but its own distinct epigenome.

The epigenome also mediates
a lifelong dialogue

between genes and the environment.

The chemical tags that
turn genes on and off

can be influenced by factors
including diet,

chemical exposure,

and medication.

The resulting epigenetic changes
can eventually lead to disease,

if, for example, they turn off a gene
that makes a tumor-suppressing protein.

Environmentally-induced epigenetic
changes are part of the reason

why genetically identical twins
can grow up to have very different lives.

As twins get older,
their epigenomes diverge,

affecting the way they age
and their susceptibility to disease.

Even social experiences can cause
epigenetic changes.

In one famous experiment,

when mother rats weren’t attentive
enough to their pups,

genes in the babies that helped them
manage stress were methylated

and turned off.

And it might not stop
with that generation.

Most epigenetic marks are erased
when egg and sperm cells are formed.

But now researchers think that some
of those imprints survive,

passing those epigenetic traits
on to the next generation.

Your mother’s or your father’s
experiences as a child,

or choices as adults,

could actually shape your own epigenome.

But even though epigenetic changes
are sticky,

they’re not necessarily permanent.

A balanced lifestyle that includes
a healthy diet,

exercise,

and avoiding exposure to contaminants

may in the long run
create a healthy epigenome.

It’s an exciting time to be studying this.

Scientists are just beginning
to understand

how epigenetics could explain mechanisms
of human development and aging,

as well as the origins of cancer,

heart disease,

mental illness,

addiction,

and many other conditions.

Meanwhile, new genome editing
techniques are making it much easier

to identify which epigenetic changes
really matter for health and disease.

Once we understand how our epigenome
influences us,

we might be able to influence it, too.

这是一个难题:

同卵双胞胎起源
于相同的 DNA,

那么

即使在具有重要
遗传成分的特征上,它们怎么会变得如此不同呢?

例如,为什么一对双胞胎
会在 55 岁时患上心脏病,

而她的妹妹却
健康地跑马拉松?

自然与后天
有很大关系,

但可以
在称为表观遗传学的东西中找到更深层次的相关答案。

这是关于 DNA 如何

与细胞内发现的大量小分子相互作用的研究

这些小分子可以激活和停用基因。

如果您将 DNA 视为一本食谱书,

那么这些分子在很大程度上决定
了何时烹饪什么。

他们自己并没有做出任何有意识的
选择,

而是他们在细胞内的存在和浓度
产生了影响。

那么这是如何工作的呢?

DNA 中的基因在被
读取并转录成 RNA 时会表达出来,RNA

通过称为核糖体的结构翻译成蛋白质。

蛋白质在很大程度上决定
了细胞的特征和功能。

表观遗传变化可以促进或
干扰特定基因的转录。

最常见的干扰发生
方式是 DNA

或它所包裹的蛋白质

被小化学标签标记。

附着在给定细胞基因组上的所有化学标签的

集合称为表观基因组。

其中一些,如甲基,

通过破坏细胞
转录机制

或导致 DNA 更紧密地盘绕,

使其难以接近,从而抑制基因表达。

基因仍然存在,但它是沉默的。

促进转录本质
上是相反的。

一些化学标签会解开 DNA,
使其更容易转录,

从而
提高相关蛋白质的产量。

表观遗传变化可以在细胞分裂中存活下来

这意味着它们可能会
影响有机体的整个生命。

有时这是一件好事。

表观遗传变化
是正常发育的一部分。

胚胎中的细胞
从一个主基因组开始。

随着细胞分裂,
一些基因被激活,

而另一些则被抑制。

随着时间的推移,通过这种表观遗传
重编程,

一些细胞发育成心脏细胞,而另一些细胞则发育

成肝细胞。 您体内

大约 200 种
细胞类型中的每一种

都具有基本相同的基因组,

但都有自己独特的表观基因组。

表观基因组还介导

基因与环境之间的终生对话。

开启和关闭基因的化学标签

可能会受到
饮食、

化学暴露

和药物等因素的影响。

由此产生的表观遗传
变化最终可能导致疾病

,例如,如果它们关闭
了制造肿瘤抑制蛋白的基因。

环境引起的表观遗传
变化是

基因相同的双胞胎
可以长大后拥有截然不同的生活的部分原因。

随着双胞胎年龄的增长,
他们的表观基因组会发生分歧,

从而影响他们的衰老方式
和对疾病的易感性。

甚至社会经历也会导致
表观遗传变化。

在一项著名的实验中,


母鼠对它们的幼崽不够关注时,

婴儿中帮助它们
管理压力的基因被甲基化

并关闭。

它可能不会
随着那一代人而停止。

当卵子和精子细胞形成时,大多数表观遗传标记被抹去。

但现在研究人员认为,其中
一些印记得以幸存,

将这些表观遗传特征
传递给下一代。

你母亲或父亲小时候的
经历,

或者成年时的选择

,实际上可以塑造你自己的表观基因组。

但即使表观遗传变化
具有粘性,

它们也不一定是永久性的。 从长远来看


包括健康饮食、

锻炼

和避免接触污染物在内的平衡生活方式

可能会
产生健康的表观基因组。

这是一个令人兴奋的时间来研究这个。

科学家们刚刚开始

了解表观遗传学如何解释
人类发育和衰老的机制,

以及癌症、

心脏病、

精神疾病、

成瘾

和许多其他疾病的起源。

与此同时,新的基因组编辑
技术

使识别哪些表观遗传变化
对健康和疾病真正重要变得更加容易。

一旦我们了解了表观基因组如何
影响我们,

我们也许也能够影响它。