Astronomers detect oldest black hole ever observed
The international team, led by the University of Cambridge, used the NASA/ESA/CSA James Webb Space Telescope (JWST) to detect the black hole, which dates from 400 million years after the big bang, more than 13 billion years ago. The results, which lead author Professor Roberto Maiolino says are “a giant leap forward”, are reported in the journal Nature.
That this surprisingly massive black hole – a few million times the mass of our Sun – even exists so early in the universe challenges our assumptions about how black holes form and grow. Astronomers believe that the supermassive black holes found at the centre of galaxies like the Milky Way grew to their current size over billions of years. But the size of this newly-discovered black hole suggests that they might form in other ways: they might be ‘born big’ or they can eat matter at a rate that’s five times higher than had been thought possible.
According to standard models, supermassive black holes form from the remnants of dead stars, which collapse and may form a black hole about a hundred times the mass of the Sun. If it grew in an expected way, this newly-detected black hole would take about a billion years to grow to its observed size. However, the universe was not yet a billion years old when this black hole was detected.
“It’s very early in the universe to see a black hole this massive, so we’ve got to consider other ways they might form,” said Maiolino, from Cambridge’s Cavendish Laboratory and Kavli Institute for Cosmology. “Very early galaxies were extremely gas-rich, so they would have been like a buffet for black holes.”
Like all black holes, this young black hole is devouring material from its host galaxy to fuel its growth. Yet, this ancient black hole is found to gobble matter much more vigorously than its siblings at later epochs.
The young host galaxy, called GN-z11, glows from such an energetic black hole at its centre. Black holes cannot be directly observed, but instead they are detected by the tell-tale glow of a swirling accretion disc, which forms near the edges of a black hole. The gas in the accretion disc becomes extremely hot and starts to glow and radiate energy in the ultraviolet range. This strong glow is how astronomers are able to detect black holes.
GN-z11 is a compact galaxy, about one hundred times smaller than the Milky Way, but the black hole is likely harming its development. When black holes consume too much gas, it pushes the gas away like an ultra-fast wind. This ‘wind’ could stop the process of star formation, slowly killing the galaxy, but it will also kill the black hole itself, as it would also cut off the black hole’s source of ‘food’.
Maiolino says that the gigantic leap forward provided by JWST makes this the most exciting time in his career. “It’s a new era: the giant leap in sensitivity, especially in the infrared, is like upgrading from Galileo’s telescope to a modern telescope overnight,” he said. “Before Webb came online, I thought maybe the universe isn’t so interesting when you go beyond what we could see with the Hubble Space Telescope. But that hasn’t been the case at all: the universe has been quite generous in what it’s showing us, and this is just the beginning.”
Maiolino says that the sensitivity of JWST means that even older black holes may be found in the coming months and years. Maiolino and his team are hoping to use future observations from JWST to try to find smaller ‘seeds’ of black holes, which may help them untangle the different ways that black holes might form: whether they start out large or they grow fast.
The research was supported in part by the European Research Council, the Royal Society, and the Science and Technology Facilities Council (STFC), part of UK Research and Innovation (UKRI).
Reference:
Roberto Maiolino et al. ‘A small and vigorous black hole in the early Universe.’ Nature (2024). DOI: 10.1038/s41586-024-07052-5
Researchers have discovered the oldest black hole ever observed, dating from the dawn of the universe, and found that it is ‘eating’ its host galaxy to death.
It’s a new era: the giant leap in sensitivity, especially in the infrared, is like upgrading from Galileo’s telescope to a modern telescope overnightRoberto MaiolinoNASA, ESA, and P. Oesch (Yale University)The GN-z11 galaxy, taken by the Hubble Space Telescope
The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.
Role of inherited genetic variants in rare blood cancer uncovered
Large-scale genetic analysis has helped researchers uncover the interplay between cancer-driving genetic mutations and inherited genetic variants in a rare type of blood cancer.
Researchers from the University of Cambridge, Wellcome Sanger Institute, and collaborators, combined various comprehensive data sets to understand the impact of both cancer-driving spontaneous mutations and inherited genetic variation on the risk of developing myeloproliferative neoplasms (MPN).
The study, published today in the journal Nature Genetics, describes how inherited genetic variants can influence whether a spontaneous mutation in a particular gene increases the risk of developing this rare blood cancer.
This analysis has an impact on current clinical predictions of disease development in individuals. Further research is required to understand the biological mechanisms behind how these inherited genetic variants influence the chances of developing rare blood cancer. In the future, this knowledge could aid drug development and interventions that reduce the risk of disease.
Myeloproliferative neoplasms, MPNs, are a group of rare, chronic, blood cancers. There are around 4,000 cases of MPN in the UK each year. These occur when the bone marrow overproduces blood cells, which can result in blood clots and bleeding. MPNs can also progress into other forms of blood cancer, such as leukaemia.
In the population, there is a large amount of natural variation between individuals’ blood cells, which can affect the amount of blood cells a person has and their particular traits. This is because multiple different genes can influence blood cell features in an individual. During routine blood tests, researchers take known information about these genes and analyse the variation to give a genetic risk score, which is how likely that individual is to develop a disease over their lifetime.
MPNs have been linked to random somatic mutations in certain genes including in a gene called JAK2. However, mutated JAK2 is commonly found in the global population, and the vast majority of these individuals do not have or go on to develop MPN.
Whilst previous studies have identified over a dozen associated inherited genetic variants that increase the risk of MPN, these studies insufficiently explain why most individuals in the population do not go on to develop MPN.
This new study, from the Wellcome Sanger Institute and collaborators, combined information on the known somatic driver mutations in MPN, inherited genetic variants, and genetic risk scores from individuals with MPN.
They found that the inherited variants that cause natural blood cell variation in the population also impact whether a JAK2 somatic mutation will go on to cause MPN. They also found that individuals with an inherited risk of having a higher blood cell count could display MPN features in the absence of cancer-driving mutations, thus, mimicking disease.
Dr Jing Guo, from the University of Cambridge and the Wellcome Sanger Institute and first author of the study, said: “Our large-scale statistical study has helped fill the knowledge gaps in how variants in DNA, both inherited and somatic, interact to influence complex disease risk. By combining these three different types of datasets we were able to get a more complete picture of how these variants combine to cause blood disorders.”
Professor Nicole Soranzo, co-senior author from the University of Cambridge, the Wellcome Sanger Institute, and Human Technopole, Italy, said: “There has been increasing realisation that human diseases have complex causes involving a combination of common and rare inherited genetic variants with different severity.
“We have previously shown that variation in blood cell parameters and function has complex genetic variability by highlighting thousands of genetic changes that affect different gene functions. Here, we show for the first time that common variants in these genes also affect blood cancers, independent of causative somatic mutations. This confirms a new important contribution of normal variability beyond complex disease, contributing to our understanding of myeloproliferative neoplasms and blood cancer more generally.”
Dr Jyoti Nangalia, co-senior author from the Wellcome-MRC Cambridge Stem Cell Institute at the University of Cambridge, and the Wellcome Sanger Institute, said: “We have a good understanding of the genetic causes of myeloproliferative neoplasms. In fact, many of these genetic mutations are routine diagnostic tests in the clinic. However, these mutations can often be found in healthy individuals without the disease.
“Our study helps us understand how inherited DNA variation from person to person can interact with cancer-causing mutations to determine whether disease occurs in the first place, and how this can alter the type of any subsequent disease that emerges. Our hope is that this information can be incorporated into future disease prediction efforts.”
This research was funded by Cancer Research UK and Wellcome.
Reference
J. Guo, K. Walter, P. M. Quiros, et al. ‘Inherited polygenic effects on common hematological traits influence clonal selection on JAK2V617F and the development of myeloproliferative neoplasms.’ Jan 2024, Nature Genetics. DOI: 10.1038/s41588-023-01638-x
Adapted from a press release by the Wellcome Sanger Institute
Combining three different sources of genetic information has allowed researchers to further understand why only some people with a common mutation go on to develop rare blood cancer
Our hope is that this information can be incorporated into future disease prediction effortsJyoti NangaliaPhoto by Sangharsh Lohakare on UnsplashDNA
The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.
Role of inherited genetic variants in rare blood cancer uncovered
Large-scale genetic analysis has helped researchers uncover the interplay between cancer-driving genetic mutations and inherited genetic variants in a rare type of blood cancer.
Researchers from the University of Cambridge, Wellcome Sanger Institute, and collaborators, combined various comprehensive data sets to understand the impact of both cancer-driving spontaneous mutations and inherited genetic variation on the risk of developing myeloproliferative neoplasms (MPN).
The study, published today in the journal Nature Genetics, describes how inherited genetic variants can influence whether a spontaneous mutation in a particular gene increases the risk of developing this rare blood cancer.
This analysis has an impact on current clinical predictions of disease development in individuals. Further research is required to understand the biological mechanisms behind how these inherited genetic variants influence the chances of developing rare blood cancer. In the future, this knowledge could aid drug development and interventions that reduce the risk of disease.
Myeloproliferative neoplasms, MPNs, are a group of rare, chronic, blood cancers. There are around 4,000 cases of MPN in the UK each year. These occur when the bone marrow overproduces blood cells, which can result in blood clots and bleeding. MPNs can also progress into other forms of blood cancer, such as leukaemia.
In the population, there is a large amount of natural variation between individuals’ blood cells, which can affect the amount of blood cells a person has and their particular traits. This is because multiple different genes can influence blood cell features in an individual. During routine blood tests, researchers take known information about these genes and analyse the variation to give a genetic risk score, which is how likely that individual is to develop a disease over their lifetime.
MPNs have been linked to random somatic mutations in certain genes including in a gene called JAK2. However, mutated JAK2 is commonly found in the global population, and the vast majority of these individuals do not have or go on to develop MPN.
Whilst previous studies have identified over a dozen associated inherited genetic variants that increase the risk of MPN, these studies insufficiently explain why most individuals in the population do not go on to develop MPN.
This new study, from the Wellcome Sanger Institute and collaborators, combined information on the known somatic driver mutations in MPN, inherited genetic variants, and genetic risk scores from individuals with MPN.
They found that the inherited variants that cause natural blood cell variation in the population also impact whether a JAK2 somatic mutation will go on to cause MPN. They also found that individuals with an inherited risk of having a higher blood cell count could display MPN features in the absence of cancer-driving mutations, thus, mimicking disease.
Dr Jing Guo, from the University of Cambridge and the Wellcome Sanger Institute and first author of the study, said: “Our large-scale statistical study has helped fill the knowledge gaps in how variants in DNA, both inherited and somatic, interact to influence complex disease risk. By combining these three different types of datasets we were able to get a more complete picture of how these variants combine to cause blood disorders.”
Professor Nicole Soranzo, co-senior author from the University of Cambridge, the Wellcome Sanger Institute, and Human Technopole, Italy, said: “There has been increasing realisation that human diseases have complex causes involving a combination of common and rare inherited genetic variants with different severity.
“We have previously shown that variation in blood cell parameters and function has complex genetic variability by highlighting thousands of genetic changes that affect different gene functions. Here, we show for the first time that common variants in these genes also affect blood cancers, independent of causative somatic mutations. This confirms a new important contribution of normal variability beyond complex disease, contributing to our understanding of myeloproliferative neoplasms and blood cancer more generally.”
Dr Jyoti Nangalia, co-senior author from the Wellcome-MRC Cambridge Stem Cell Institute at the University of Cambridge, and the Wellcome Sanger Institute, said: “We have a good understanding of the genetic causes of myeloproliferative neoplasms. In fact, many of these genetic mutations are routine diagnostic tests in the clinic. However, these mutations can often be found in healthy individuals without the disease.
“Our study helps us understand how inherited DNA variation from person to person can interact with cancer-causing mutations to determine whether disease occurs in the first place, and how this can alter the type of any subsequent disease that emerges. Our hope is that this information can be incorporated into future disease prediction efforts.”
This research was funded by Cancer Research UK and Wellcome.
Reference
J. Guo, K. Walter, P. M. Quiros, et al. ‘Inherited polygenic effects on common hematological traits influence clonal selection on JAK2V617F and the development of myeloproliferative neoplasms.’ Jan 2024, Nature Genetics. DOI: 10.1038/s41588-023-01638-x
Adapted from a press release by the Wellcome Sanger Institute
Combining three different sources of genetic information has allowed researchers to further understand why only some people with a common mutation go on to develop rare blood cancer
Our hope is that this information can be incorporated into future disease prediction effortsJyoti NangaliaPhoto by Sangharsh Lohakare on UnsplashDNA
The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.