Partes del genoma sin función conocida podrían participar en la formación de nuevas proteínas. Una nueva investigación ha identificado casi 2.500 lncRNAs que no constan en las bases de datos. La mayoría de los lncRNAs están solo en una sola especie, lo que indica que tienen un origen reciente.El hallazgo más importante es que, en todas las especies, una fracción importante de los lncRNAs se asocia a la maquinaria celular que sintetiza proteínas a partir de ARN. Así pues, en contra de la opinión dominante, muchos lncRNAs podrían producir proteínas. El estudio de especies cercanas permitirá entender mejor los procesos de formación de nuevos genes codificantes. / Fotolia Showing image 1 of 1 Los ribosomas fabrican proteínas a partir de las instrucciones que hay en la molécula de ARN. Ahora, una nueva técnica de secuenciación ha revelado que muchos de estos transcritos (lncRNA) también podrían traducirse en proteínas, lo que está siendo objeto de un intenso debate.
Referencia bibliográfica: Investigadores identifican tres nuevos genes implicados en el desarrollo de la esclerodermia – Genética – Noticias, última hora, vídeos y fotos de Genética en lainformacion.com. Un estudio internacional, coliderado por el Consejo Superior de Investigaciones Científicas (CSIC), ha identificado tres nuevos genes implicados en el desarrollo de la esclerosis sistémica o esclerodermia, permitiendo así elevar a 17 el número de genes de riesgo involucrados en esta enfermedad. Para llevar a cabo el trabajo, publicado en la revista 'American Journal of Human Genetics', los expertos analizaron a más de 5.800 pacientes y 9.400 personas que no estaban afectadas. Además, estudiaron aproximadamente 200.000 variantes genéticas localizadas en 186 genes relacionados con diferentes trastornos autoinmunes.
"Confiamos en que la identificación del entramado genético que contribuye al inicio y desarrollo de la enfermedad pueda traducirse en el futuro en terapias específicas y medicina personalizada", ha asegurado la investigadora del CSIC y miembro del Instituto de Parasitología y Biomedicina López-Neyra en Granada, Lara Bossini. (EuropaPress) Human brain gene Foxp2 makes mice smarter in some ways. Although it's far from the sort of brain transplant beloved by science fiction enthusiasts, scientists have taken one step in that direction: they have spliced a key human brain gene into mice. In the first study designed to assess how partially "humanizing" brains of a different species affects key cognitive functions, scientists reported on Monday that mice carrying a human gene associated with language learned new ways to find food in mazes faster than normal mice. By isolating the effects of one gene, the work sheds light on its function and hints at the evolutionary changes that led to the unique capabilities of the human brain.
For the study, scientists used hundreds of mice genetically engineered to carry the human version of Foxp2, a gene linked to speech and language. In a 2009 study, mice carrying human Foxp2 developed more-complex neurons and more-efficient brain circuits. Summary of the paper in PNAS. 'Smart genes' prove elusive. Jirsak/Shutterstock Researchers found 69 genes that correlate with higher educational attainment — and three of those also also appear to have a direct link to slightly better cognitive abilities. Scientists looking for the genes underlying intelligence are in for a slog. One of the largest, most rigorous genetic study of human cognition1 has turned up inconclusive findings, and experts concede that they will probably need to scour the genomes of more than 1 million people to confidently identify even a small genetic influence on intelligence and other behavioural traits.
Studies of twins have repeatedly confirmed a genetic basis for intelligence, personality and other aspects of behaviour. But efforts to link IQ to specific variations in DNA have led to a slew of irreproducible results. Critics have alleged that some of these studies' methods were marred by wishful thinking and shoddy statistics. The researchers picked out 69 gene variants most strongly linked to education level. Biologists delay the aging process by ‘remote control’ UCLA biologists have identified a gene that can slow the aging process throughout the entire body when activated remotely in key organ systems. Working with fruit flies, the life scientists activated a gene called AMPK that is a key energy sensor in cells; it gets activated when cellular energy levels are low. Increasing the amount of AMPK in fruit flies’ intestines increased their lifespans by about 30 percent — to roughly eight weeks from the typical six — and the flies stayed healthier longer as well.
“We have shown that when we activate the gene in the intestine or the nervous system, we see the aging process is slowed beyond the organ system in which the gene is activated,” Walker said. Walker said that the findings are important because extending the healthy life of humans would presumably require protecting many of the body’s organ systems from the ravages of aging — but delivering anti-aging treatments to the brain or other key organs could prove technically difficult. Three gene networks discovered in autism, may present treatment targets. A large new analysis of DNA from thousands of patients has uncovered several underlying gene networks with potentially important roles in autism. These networks may offer attractive targets for developing new autism drugs or repurposing existing drugs that act on components of the networks.
Furthermore, one of the autism-related gene pathways also affects some patients with attention-deficit hyperactivity disorder (ADHD) and schizophrenia—raising the possibility that a class of drugs may treat particular subsets of all three neurological disorders. “Neurodevelopmental disorders are extremely heterogeneous, both clinically and genetically,” said study leader Hakon Hakonarson, M.D., Ph.D., director of the Center for Applied Genomics at The Children’s Hospital of Philadelphia (CHOP).
“However, the common biological patterns we are finding across disease categories strongly imply that focusing on underlying molecular defects may bring us closer to devising therapies.” The Mitochondrial Epigenetic Revolution: A New Avenue for Potential Research. Is Musical Talent Rooted in Genes? Practice doesn't always make perfect when it comes to becoming the next Mozart, a new study suggests. Researchers compared pairs of identical twins, and found that no matter how hard one twin had practiced up until that point in their life, the other twin who had practiced much less still had an equal level of ability in certain musical skills.
This may be because some aspects of musical talent are built into the genes, the researchers said. "The idea that an externally imposed practice regime can and will lead to expertise seems to be wrong," said study researcher Miriam Mosey, a neuroscientist at the Karolinska Institute in Sweden. "But innate ability should also not be seen in a deterministic way, as, naturally, practice will (almost) always lead to an increase in ability (but not necessarily to high-level expertise)," she said in an email to Live Science. [Seeing Double: 8 Fascinating Facts About Twins] Grandma's Experiences Leave Epigenetic Mark on Your Genes. Why can’t your friend “just get over” her upbringing by an angry, distant mother? Why can’t she “just snap out of it”? The reason may well be due to methyl groups that were added in childhood to genes in her brain, thereby handcuffing her mood to feelings of fear and despair. Of course, it is generally not possible to sample the brains of living people.
But examining blood samples in humans is routine, and Szyf has gone searching there for markers of epigenetic methylation. Sure enough, in 2011 he reported on a genome-wide analysis of blood samples taken from 40 men who participated in a British study of people born in England in 1958. All the men had been at a socioeconomic extreme, either very rich or very poor, at some point in their lives ranging from early childhood to mid-adulthood.
In all, Szyf analyzed the methylation state of about 20,000 genes. Timing, in other words, matters. The Mark Of Cain. The Science of Laziness. Strict genomic partitioning by biological clock separates key metabolic functions. Much of the liver's metabolic function is governed by circadian rhythms – our own body clock – and UC Irvine researchers have now found two independent mechanisms by which this occurs. The study, published online today in Cell, reveals new information about the body clock's sway over metabolism and points the way to more focused drug treatments for liver disease and such metabolic disorders as obesity and diabetes. Paolo Sassone-Corsi, UCI's Donald Bren Professor of Biological Chemistry, and postdoctoral scholar Selma Masri report that two of these circadian-linked proteins, SIRT1 and SIRT6, manage important liver processes – lipid storage and energy usage in liver cells – separately and distinctly from each other.
This surprising discovery of genomic partitioning, Masri noted, reveals how strictly regulated circadian control of metabolism can be. "The ability of the genome and epigenome to cross-talk with metabolic pathways is critical for cellular and organismal functions. New regions of genetic material are involved in the development of colon cancer. Most research on human cancer genes have been focused on the regions of the coding genome (exons) that are to be translated in the form of amino acids thus proteins. But just before each gene, there is a regulatory region or activator which controls the expression and activity of the adjacent gene.
Until now, very little was known of the role exerted such DNA fragment in tumor development. An article published today in Nature in collaboration with the group of Manel Esteller, Director of Epigenetics and Cancer Biology, Bellvitge Biomedical Research Institute (IDIBELL), ICREA researcher and Professor of Genetics at the University of Barcelona, shows that these regions are also altered in cancer.
"The results of the Nature study reveal that regulatory regions preceding the gene as such, are variable, can mutate and be chemically modified, such as with DNA methylation in the cells of the tumor transformation" declares Esteller, co -author of the study. New Schizophrenia Gene Links Uncovered. A new genetic analysis of people with schizophrenia — and the largest study investigating the genetic basis of any psychiatric disorder to date — provides hints that the disease may sometimes be connected with infections as some researchers have long suggested.
These findings could one day lead to new therapies for people with schizophrenia, scientists said. There have been few innovative drug treatments for schizophrenia over the last 60 years. "In the past, people thought schizophrenia must happen because of some really bad mutations in a person not seen in people around them," said study co-author Steve McCarroll, director of genetics at the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard in Cambridge, Massachusetts. "This study shows a substantial part of the risk of schizophrenia comes from many tiny nudges to the genome that all humans share. " The genetics of schizophrenia What these genes do. 100% Success in Gene Reprogramming – The Weizmann Wave. First, there was the great hope of induced pluripotent stem cells (iPSCs), and then there was the inevitable letdown. When the announcement came, in 2006, that simple adult skin cells could be reprogrammed – reverted back to an embryonic stem cell state by the addition of just four genes – it seemed like an almost magical solution to the problems of using stem cells from embryos.
But then some studies started to find that the reprogramming process was not perfect – iPSCs were similar, but not identical, to the cells from early embryos. More critically, only about 1% of the cells treated with the four-gene combination actually turn into iPSCs, and the process is painstakingly slow – around four weeks. That is just fine for a research lab, not so great for developing medical applications. Of course, labs everywhere have been working to improve the process. Dr. Left: Combined image of skin cells (red) and reprogrammed cells in the previous method (green) shows very few iPSCs. Descobreixen quan va aparèixer el gen dels pèl-roigs.
Abstract | Efficient utilization of aerobic metabolism helps Tibetan locusts conquer hypoxia. Research article Dejian Zhao1, Zhenyu Zhang1, Arianne Cease2, Jon Harrison2 and Le Kang1* * Corresponding author: Le Kang lkang@ioz.ac.cn Author Affiliations 1 State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing, China 2 School of Life Sciences, Arizona State University, Tempe, AZ, USA For all author emails, please log on.
BMC Genomics 2013, 14:631 doi:10.1186/1471-2164-14-631 Published: 18 September 2013 Abstract Background Responses to hypoxia have been investigated in many species; however, comparative studies between conspecific geographical populations at different altitudes are rare, especially for invertebrates. Results Here we compared the hypoxic responses of TP and NP locusts from morphological, behavioral, and physiological perspectives. Conclusions Our results indicate that TP and NP locusts have undergone divergence in hypoxia tolerance.
Keywords: Hypoxia; Microarray; Locusta migratoria; Tibet close.