{"id":2220,"date":"2024-09-12T22:59:53","date_gmt":"2024-09-12T20:59:53","guid":{"rendered":"https:\/\/kleefstrasyndrome.com\/?p=2220"},"modified":"2026-08-20T16:42:43","modified_gmt":"2026-08-20T14:42:43","slug":"ehmt1-variants-kleefstra-spectrum-2024","status":"publish","type":"post","link":"https:\/\/kleefstrasyndrome.com\/en\/ehmt1-variants-kleefstra-spectrum-2024\/","title":{"rendered":"Kleefstra syndrome is broader than previously thought: what the largest EHMT1 study in 209 individuals showed"},"content":{"rendered":"
\n

For many years, the classic description of Kleefstra syndrome was based primarily on individuals with a relatively characteristic clinical picture: developmental delay, moderate to severe intellectual disability, hypotonia, significant speech and communication difficulties, and characteristic morphological features.<\/p>\n\n\n\n

However, as genetic diagnosis evolves and exome and genome sequencing is used in more and more people, variations are being identified in EHMT1<\/strong> and to individuals who do not necessarily fit the \u00abclassic\u00bb image of the syndrome.<\/p>\n\n\n\n

In 2024, a large international team led by Dmitrijs Rots<\/strong>, and with the participation of Tjitske Kleefstra<\/strong> and dozens of researchers and clinicians from many countries, published in American Journal of Human Genetics<\/em> one of the most important studies conducted to date on KLEFS1. The researchers gathered 209 people with a rare genetic variant in EHMT1<\/strong> and combined clinical data, computational analysis, laboratory functional tests, and study of the DNA methylation pattern. After overall evaluation, the variants 191 people<\/strong> classified or reclassified as likely pathogenic or pathogenic, molecularly confirming KLEFS1.<\/p>\n\n\n\n

The size of the study matters. This is not simply a collection of new cases, but an effort to answer a much more difficult question:<\/p>\n\n\n\n

Why can two people with mutations in the same gene have such different clinical presentations?;<\/strong><\/p>\n\n\n\n

From \u00abwhat the syndrome looks like\u00bb to \u00abwhat the genetic change actually does\u00bb<\/h2>\n\n\n\n

Traditionally, many genetic syndromes were recognized using a phenotype-first approach: doctors observed a specific set of features and then searched for the genetic cause.<\/p>\n\n\n\n

Today, the reverse is happening more and more often. Genetic testing first identifies a mutation, and then researchers try to figure out whether it actually causes disease and what the spectrum of its manifestations might be.<\/p>\n\n\n\n

This change proved particularly important for Kleefstra. The study by Rots and colleagues showed that KLEFS1 may present with much broader range of cognitive and developmental characteristics<\/strong> than what older patient series described. In the new group, there were even individuals with normal cognitive function<\/strong>, something that was previously not considered representative of the classical picture of the syndrome.<\/p>\n\n\n\n

This does not mean that severe developmental burden ceases to be an important part of KLEFS1. But it means that the name of the diagnosis alone does not tell us how severe the condition of a specific person will be<\/strong>.<\/p>\n\n\n\n

EHMT1 does not have a single function<\/h2>\n\n\n\n

To understand one of the most important findings of the work, we need to take a closer look at what the EHMT1<\/strong>.<\/p>\n\n\n\n

The gene encodes a protein involved in the regulation of gene expression through epigenetic mechanisms. In cooperation with EHMT2, it is involved, among other things, in the methylation of histone H3 at lysine 9 \u2014 a mechanism that contributes to regulating which genes will be more or less active.<\/p>\n\n\n\n

However, the protein has different functional regions. Two of the most important are:<\/p>\n\n\n\n

the ANKR (ankyrin repeat domain) region<\/strong> and
the SET area<\/strong>.<\/p>\n\n\n\n

To put it simply, ANKR is involved in \u00abreading\u00bb epigenetic marks\u2014which is why the authors speak of reader function<\/strong> \u2014 while the SET domain possesses the catalytic activity of methyltransferase, meaning it acts as writer<\/strong>.<\/p>\n\n\n\n

The study's major contribution was showing that Not all EHMT1 variations have the same biological effect<\/strong>.<\/p>\n\n\n\n

The ANKR region seems to be of particular importance for KLEFS1<\/h2>\n\n\n\n

Researchers thoroughly studied variants that alter protein structure, including missense and small in-frame changes.<\/p>\n\n\n\n

When such a variation disrupted the \u00abreading\u00bb function of the region ANKR<\/strong>, individuals showed the characteristic DNA methylation pattern associated with KLEFS1 and generally a milder form of the Kleefstra phenotype<\/strong> compared to classic full loss-of-function variants.<\/p>\n\n\n\n

Conversely, when a change substantially affected only the catalytic \u201cwriter\u201d function of the SET domain<\/strong>, the researchers saw neither the characteristic methylation pattern of KLEFS1 nor the typical clinical picture of the syndrome.<\/p>\n\n\n\n

This is a particularly interesting finding, because it distances us from the oversimplified idea that:<\/p>\n\n\n\n

\u00abany damage to EHMT1 is equivalent to Kleefstra itself.<\/strong><\/p>\n\n\n\n

Reality seems more complex.<\/p>\n\n\n\n

What does Kleefstra \u00abmethylation signature\u00bb mean?;<\/h2>\n\n\n\n

Another important tool of the study was the analysis of DNA methylation<\/strong>.<\/p>\n\n\n\n

Certain genetic syndromes affecting epigenetic mechanisms leave a relatively characteristic methylation pattern at many genomic loci. This is often called DNA methylation episignature<\/strong>.<\/p>\n\n\n\n

We can think of it as a molecular \u00abfingerprint\u00bb that helps researchers figure out whether a genetic variant has actually caused the functional disorder expected for the specific syndrome.<\/p>\n\n\n\n

In the study by Rots et al., this was particularly useful for variants whose clinical significance was not clear from the outset. The researchers therefore did not limit themselves to the question \u00abis there a change in DNA?\u00bb, but tried to determine if the change actually affects protein function and leaves the expected epigenetic footprint<\/strong>.<\/p>\n\n\n\n

At the same time, the study also demonstrates something important: the absence of the classic episignature in certain variant categories should not be interpreted without taking into account the precise molecular mechanism and functional data.<\/p>\n\n\n\n

There are also much milder forms<\/h2>\n\n\n\n

Another category that stood out was certain N-terminal truncating variants<\/strong>, meaning changes that cause premature termination near the beginning of the protein.<\/p>\n\n\n\n

Researchers observed that these could connect to milder neurodevelopmental phenotype<\/strong> without the characteristic methylation pattern of KLEFS1.<\/p>\n\n\n\n

On the other hand, in the group with the classic alterations that essentially lead to a loss of function of EHMT1, the clinical picture was closer to what we traditionally know as Kleefstra. In this subgroup, 94%<\/strong> had an intellectual disability or learning difficulties and 98%<\/strong> developmental delay. Of the 12 individuals for whom numerical IQ data were available, the average was 54.<\/p>\n\n\n\n

However, these numbers describe a group of people; cannot be used to predict the progress of a specific child<\/strong>.<\/p>\n\n\n\n

Kleefstra can be inherited<\/h2>\n\n\n\n

A finding of particular importance for genetic counseling was the identification KLEFS1 multi-family cases<\/strong>, in which a pathogenic variant had been inherited from a parent.<\/p>\n\n\n\n

KLEFS1 is still frequently associated with new, de novo variants. However, the new study shows that the picture is more complex: a parent carrying a pathogenic variant may have much milder phenotype<\/strong>, to the point that the diagnosis had not been previously recognized.<\/p>\n\n\n\n

This has significant practical consequence.<\/p>\n\n\n\n

When an EHMT1 variant is identified in a child and is also present in a parent, the fact that the parent appears to be functioning well it is not enough on its own to classify the variant as harmless<\/strong>. The authors emphasize the importance of detailed assessment and of the parents, particularly in familial cases.<\/p>\n\n\n\n

New image for behavior and mental health as well<\/h2>\n\n\n\n

The large team allowed researchers to get a better look at features that might have been underestimated in older descriptions.<\/p>\n\n\n\n

In individuals aged 5 years and older for whom relevant data were available, a wide range of behavioral and psychiatric manifestations was recorded. The researchers found that such difficulties are not necessarily limited to adolescence or adulthood<\/strong>, but they can already be present in childhood.<\/p>\n\n\n\n

The same analysis recorded, among other things, autism spectrum disorder, anxiety, aggressive behavior, mood disorders, and in some individuals loss of previously acquired skills or functional regression<\/strong>.<\/p>\n\n\n\n

This does not mean that all these manifestations will present in every person with Kleefstra. Instead, one of the central messages of the entire work is precisely the high individual variability<\/strong>.<\/p>\n\n\n\n

Some physical problems might be more common than we thought<\/h2>\n\n\n\n

The study also allowed a more modern assessment of certain clinical characteristics.<\/p>\n\n\n\n

The authors state that constipation<\/strong> was recorded at approximately 47% for the group; the recurrent infections<\/strong> at approximately 46%, and the sleep-wake disorders<\/strong> also at approximately 46%. Furthermore, atrophy or hypoplasia of brain structures had been recorded at approximately 29% in individuals for whom relevant data were available.<\/p>\n\n\n\n

These percentages require proper interpretation. They do not constitute a prediction for every child, nor do they mean that every individual should be tested for everything regardless of symptoms and medical history. However, they do show which issues are worth knowing for clinicians monitoring people with KLEFS1.<\/p>\n\n\n\n

How common is Kleefstra syndrome after all?;<\/h2>\n\n\n\n

Another interesting result was the new estimate of the frequency of KLEFS1.<\/p>\n\n\n\n

Based on their data, the researchers calculated that the frequency may be around:<\/p>\n\n\n\n

1 person per 36,000.<\/strong><\/p>\n\n\n\n

This is about estimate<\/strong> and not for an absolutely recorded number of people with the diagnosis. However, it is significantly higher than some older estimates and supports the idea that KLEFS1 likely remains underdiagnosed<\/strong>, especially in milder cases. The estimate of approximately 1:36,000 was later adopted in international clinical guidelines for the syndrome.<\/p>\n\n\n\n

\n

What does this study change for families?;<\/h2>\n\n\n\n

Perhaps the most important message of the study is that Kleefstra syndrome it does not constitute a single, predetermined developmental path<\/strong>.<\/p>\n\n\n\n

The diagnosis identifies the genetic cause, but cannot by itself accurately predict:<\/p>\n\n\n\n

when a child will walk or talk, how much they will develop their language, what their level of cognitive function will be, whether they will develop epilepsy, behavioral or psychiatric difficulties, or what the degree of their independence will be in adult life.<\/p>\n\n\n\n

The work of Rots et al. shows that even within the same gene there are different molecular mechanisms<\/strong> which can lead to a different phenotype.<\/p>\n\n\n\n

And this perhaps explains a part of what families have been seeing for years: two children with KLEFS1 may resemble each other in certain characteristics and at the same time be strikingly different in others.<\/p>\n<\/div><\/div>\n\n\n\n

\n

Almost 20 years after the discovery of EHMT1<\/h2>\n\n\n\n

In 2006, the functional loss of EHMT1<\/strong> recognized as the root cause of the syndrome we now know as Kleefstra type 1.<\/p>\n\n\n\n

Almost two decades later, the study by Rots and colleagues shows how much our understanding has evolved.<\/p>\n\n\n\n

It is no longer enough to ask:<\/p>\n\n\n\n

\u00abIs there a change in EHMT1?\u00bb<\/strong><\/p>\n\n\n\n

Researchers can gradually ask much more specific questions:<\/p>\n\n\n\n

Which change? At which point in the protein? Which function does it affect? Does it cause a loss of function? Does it affect the ANKR or the SET domain? Is the characteristic epigenetic signature present? And how do all these connect to the human clinical picture?;<\/strong><\/p>\n\n\n\n

This deeper understanding is important both for more accurate genetic diagnosis and counseling and for the future of research.<\/p>\n\n\n\n

For families, however, perhaps the most important conclusion can be stated much more simply:<\/p>\n\n\n\n

Kleefstra syndrome has a much greater diversity than we previously knew. Genetic diagnosis is important, but it is not in itself a prediction of a child's potential and course.<\/strong><\/p>\n<\/div><\/div>\n\n\n\n

\n

Sources and related bibliography<\/h3>\n\n\n\n

Rots D, Bouman A, Yamada A, et al.<\/strong> Comprehensive EHMT1 variants analysis broadens genotype-phenotype associations and molecular mechanisms in Kleefstra syndrome.<\/em> American Journal of Human Genetics. 2024;111(8):1605\u20131625. doi:10.1016\/j.ajhg.2024.06.008<\/a>.<\/p>\n\n\n\n

Bouman A, et al.<\/strong> International clinical evidence-based guideline for Kleefstra syndrome.<\/em> Genetics in Medicine. 2026. Subsequent international guidelines also use the modern prevalence estimate of approximately 1:36,000.<\/p>\n<\/div><\/div>\n<\/div><\/div>","protected":false},"excerpt":{"rendered":"

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