Amazing new research has shown that we can detect what species of fish are found in different parts of our seas simply by collecting samples of the local seawater. The key to identifying which species are present is in traces of DNA - known as environmental DNA (eDNA) - which are left in the surrounding water by fish that pass through. Just half a litre of seawater from a temperate marine ecosystem in Denmark provided DNA fragments from 15 different fish species, including some that were rarely recorded by more invasive conventional methods, as well as 4 bird species. Experiments show that even small fragments of eDNA degrade to the point that they are no longer detectable within days, suggesting that the method gives an up-to-date and accurate recording of the species that inhabit the area at that point in time. A further study looking into the possibility of marine mammal detection using the eDNA method suggests that greater volumes of seawater are needed to be analysed in order to detect them, but that eDNA has the potential to support current visual and acoustic methods of species detection for marine mammals as well as fish.Ref: Thomsen P. F. et al., 2012. Detection of a diverse marine fish fauna using environmental DNA from seawater samples. PLOS One [link]Foote A. D. et al., 2012. Investigating the potential use of environmental DNA (eDNA) for genetic monitoring of marine mammals. PLOS One [link] 

Amazing new research has shown that we can detect what species of fish are found in different parts of our seas simply by collecting samples of the local seawater. The key to identifying which species are present is in traces of DNA - known as environmental DNA (eDNA) - which are left in the surrounding water by fish that pass through. Just half a litre of seawater from a temperate marine ecosystem in Denmark provided DNA fragments from 15 different fish species, including some that were rarely recorded by more invasive conventional methods, as well as 4 bird species. Experiments show that even small fragments of eDNA degrade to the point that they are no longer detectable within days, suggesting that the method gives an up-to-date and accurate recording of the species that inhabit the area at that point in time. A further study looking into the possibility of marine mammal detection using the eDNA method suggests that greater volumes of seawater are needed to be analysed in order to detect them, but that eDNA has the potential to support current visual and acoustic methods of species detection for marine mammals as well as fish.

Ref: Thomsen P. F. et al., 2012. Detection of a diverse marine fish fauna using environmental DNA from seawater samples. PLOS One [link]
Foote A. D. et al., 2012. Investigating the potential use of environmental DNA (eDNA) for genetic monitoring of marine mammals. PLOS One [link



It is a well-known phenomenon that within mammalian species, females tend to outlive males. The male sex hormone testosterone not only puts males at behavioural risk of injury in terms of aggression and competitiveness (as well as involving high energy expenditure), but also increases levels of harmful LDL cholesterol in the blood, leading to a greater risk of heart disease and stroke. As such, a broad variety of immune-related genes may be more important in males than it is in females. Researchers studying the Alpine chamois (Rupicapra rupicapra) have recently investigated this hypothesis. Observing wild chamois living in the eastern Alps, scientists discovered that in areas affected by scabies, reproductive-age males had a higher death rate than both females and younger males. They noted that mature males depleted their fat stores at the end of the winter around 6 weeks earlier than females and younger males, presumably due to the large amount of energy expended in rutting. Lower fat reserves leave less energy for maintaining a strong immune system. Researchers wanted to know whether variation in genes that influenced immune response could improve male probability of survival.The scientists chose to examine a gene called MHC class II DRB from what is known as the major histocompatibility complex (MHC). This is a set of around 128 active genes along with 96 non-functional pseudogenes that have an important role in the immune system. The MHC shows huge variation between individuals - 100 times greater than the genome average, giving a 10% difference between any two unrelated individuals. These variations seem to correspond with differences in susceptibility to a whole host of diseases such as malaria, tuberculosis and HIV/AIDS.In areas affected by scabies, the proportion of males that were heterozygous (had two different copies of the gene) increased with age, implying that homozygous individuals (those with two identical copies of the gene) had higher mortality rates. Male individuals heterozygous at the locus were indeed found to survive significantly longer than homozygous individuals - but this did not apply in females. The research supports the theory that when the immune system is compromised, heterozygosity in immune genes increases male chances of survival.Ref:  Schaschl H., Suchentrunk F., Morris D. L. et al., 2012. Sex-specific selection for MHC variability in Alpine chamois. BMC Evolutionary Biology 12:20 [link]Twyman R., 2003. The major histocompatibility complex. Wellcome Trust: The Human Genome [link]

It is a well-known phenomenon that within mammalian species, females tend to outlive males. The male sex hormone testosterone not only puts males at behavioural risk of injury in terms of aggression and competitiveness (as well as involving high energy expenditure), but also increases levels of harmful LDL cholesterol in the blood, leading to a greater risk of heart disease and stroke. As such, a broad variety of immune-related genes may be more important in males than it is in females. Researchers studying the Alpine chamois (Rupicapra rupicapra) have recently investigated this hypothesis. Observing wild chamois living in the eastern Alps, scientists discovered that in areas affected by scabies, reproductive-age males had a higher death rate than both females and younger males. They noted that mature males depleted their fat stores at the end of the winter around 6 weeks earlier than females and younger males, presumably due to the large amount of energy expended in rutting. Lower fat reserves leave less energy for maintaining a strong immune system. Researchers wanted to know whether variation in genes that influenced immune response could improve male probability of survival.

The scientists chose to examine a gene called MHC class II DRB from what is known as the major histocompatibility complex (MHC). This is a set of around 128 active genes along with 96 non-functional pseudogenes that have an important role in the immune system. The MHC shows huge variation between individuals - 100 times greater than the genome average, giving a 10% difference between any two unrelated individuals. These variations seem to correspond with differences in susceptibility to a whole host of diseases such as malaria, tuberculosis and HIV/AIDS.

In areas affected by scabies, the proportion of males that were heterozygous (had two different copies of the gene) increased with age, implying that homozygous individuals (those with two identical copies of the gene) had higher mortality rates. Male individuals heterozygous at the locus were indeed found to survive significantly longer than homozygous individuals - but this did not apply in females. The research supports the theory that when the immune system is compromised, heterozygosity in immune genes increases male chances of survival.

Ref:  Schaschl H., Suchentrunk F., Morris D. L. et al., 2012. Sex-specific selection for MHC variability in Alpine chamois. BMC Evolutionary Biology 12:20 [link]
Twyman R., 2003. The major histocompatibility complex. Wellcome Trust: The Human Genome [link]



For a long time, the history of the domestication of the horse has been a muddled one. While archaeological evidence suggests that the domestic horse (Equus caballus) originated in the western Eurasian steppes (Ukraine, southwest Russia and west Kazakhstan), a large variety of female lineages in the gene pool contradicts this, implying not a single origin but instead multiple domestication events. An important unanswered question was whether the spread of horse domestication around the world involved the actual movement of herds from a specific geographic origin, known as ‘demic spread’, or whether it simply involved passing on successful techniques so that people in other regions could domesticate their own local wild horses, resulting in multiple domestication events from numerous different populations. New research that has analysed mitochondrial DNA and Y-chromosomes from a genetic database of over 300 horses has finally resolved the answers to these questions. The data has traced the origins of domestic horses to a single ancestral population of Equus ferus (now extinct) that was indeed living in the western Eurasian steppes from at least 160,000 years ago. Humans first domesticated the horse in this region around 4000 B.C., and from here domesticated horses spread outwards across Europe and Asia, in the process of which stock was supplemented with local wild horses in different regions. These wild horses that were bred into domestic herds were the source of the new female lineages that we can identify in the gene pool today.Ref: Warmuth V., Eriksson A., Bower M. A., Barker G., Barrett E. et al., 2012. Reconstructing the origin and spread of horse domestication in the Eurasian steppe. PNAS Online [link]

For a long time, the history of the domestication of the horse has been a muddled one. While archaeological evidence suggests that the domestic horse (Equus caballus) originated in the western Eurasian steppes (Ukraine, southwest Russia and west Kazakhstan), a large variety of female lineages in the gene pool contradicts this, implying not a single origin but instead multiple domestication events. An important unanswered question was whether the spread of horse domestication around the world involved the actual movement of herds from a specific geographic origin, known as ‘demic spread’, or whether it simply involved passing on successful techniques so that people in other regions could domesticate their own local wild horses, resulting in multiple domestication events from numerous different populations. New research that has analysed mitochondrial DNA and Y-chromosomes from a genetic database of over 300 horses has finally resolved the answers to these questions. The data has traced the origins of domestic horses to a single ancestral population of Equus ferus (now extinct) that was indeed living in the western Eurasian steppes from at least 160,000 years ago. Humans first domesticated the horse in this region around 4000 B.C., and from here domesticated horses spread outwards across Europe and Asia, in the process of which stock was supplemented with local wild horses in different regions. These wild horses that were bred into domestic herds were the source of the new female lineages that we can identify in the gene pool today.

Ref: Warmuth V., Eriksson A., Bower M. A., Barker G., Barrett E. et al., 2012. Reconstructing the origin and spread of horse domestication in the Eurasian steppe. PNAS Online [link]



Research using mice has revealed a new gene that plays an essential role in mammalian fertility: the PDILT gene encodes a protein that enables sperm to navigate their way through the oviduct and bind correctly to the egg during the process of fertilisation. The PDILT protein stimulates the correct folding of another protein called ADAM3, which is then localised to the outer membrane of the sperm. Without PDILT, the ADAM3 protein is not folded correctly or transported to where it is needed to be. Its critical importance was evident following the discovery that if its expression is ‘switched off’ in sperm, fewer than 3% of eggs become fertilised, in comparison with approximately 80% when the gene is active. Sperm lacking PDILT are not only unable to bind the egg fully, but find it difficult to navigate through the oviduct to get to it in the first place. The experiments also revealed that what are known as cumulus cells, which form a protective layer around the egg, aid in effective binding of the sperm to the egg and will help to rescue the binding difficulties caused by the absence of PDILT, enabling successful fertilisation. The next step will be to examine how the gene works in humans - from there, it may be possible to produce fertility treatments that could aid in making IVF more successful for those couples that are faced with low fertility.Ref: Durham University, 2012. Gene involved in sperm-to-egg binding is key to fertility in mammals. EurekAlert! News [link]

Research using mice has revealed a new gene that plays an essential role in mammalian fertility: the PDILT gene encodes a protein that enables sperm to navigate their way through the oviduct and bind correctly to the egg during the process of fertilisation. The PDILT protein stimulates the correct folding of another protein called ADAM3, which is then localised to the outer membrane of the sperm. Without PDILT, the ADAM3 protein is not folded correctly or transported to where it is needed to be. Its critical importance was evident following the discovery that if its expression is ‘switched off’ in sperm, fewer than 3% of eggs become fertilised, in comparison with approximately 80% when the gene is active. Sperm lacking PDILT are not only unable to bind the egg fully, but find it difficult to navigate through the oviduct to get to it in the first place. The experiments also revealed that what are known as cumulus cells, which form a protective layer around the egg, aid in effective binding of the sperm to the egg and will help to rescue the binding difficulties caused by the absence of PDILT, enabling successful fertilisation. The next step will be to examine how the gene works in humans - from there, it may be possible to produce fertility treatments that could aid in making IVF more successful for those couples that are faced with low fertility.

Ref: Durham University, 2012. Gene involved in sperm-to-egg binding is key to fertility in mammals. EurekAlert! News [link]