Mendel’s law of segregation states that during the gametes production the two copies of each hereditary factor separate so that progeny receive one factor from each parent.
Observing that breeding pea plant with different traits gave rise to F1 generations in which all the plants expressed the dominant trait and F2 generation in which some plants expressed the recessive and dominant traits in the ratio of 1:3, Mendel proposed the law of segregation. According to that law, each individual that is diploid have a pair of alleles for a particular trait. At random, each parent passes an allele to their progeny resulting in a diploid organism. The allele with the dominant trait determines the offspring phenotype. In essence, the law of segregation states that copies of gene segregate or separate so that each gamete gets only one allele.
The physical basis of the law of segregation is the 1st division of meiosis where the homologous chromosomes with versions of each gene are separated into daughter nucleic. The homologous chromosomes behaviour during meiosis accounts for the separation of the alleles to different gametes. As the chromosome separate into different gametes, the two alleles for a particular gene also separate so that each gamete receives one of the two alleles.
Since human cells have two copies of each chromosome, they carry two versions of each gene. Different gene versions are known as alleles. Depending on their associated characteristics, alleles are either dominant or recessive.
Dominant alleles display their effect even when an individual only carry one copy of the allele. This condition is referred to as being heterozygous. For instance, since the allele for brown eyes is dominant, an individual only need one allele for the brown eye to have brown eyes. An individual with two copies of the ‘brown eye’ allele will still have brown eyes.
Recessive alleles only display their effect if an organism has two copies of the allele. This condition is also known as being homozygous. For example, blue eyes allele is recessive. Therefore, for an individual to have blue eyes, he/she needs to have two copies of allele for the blue eyes. Another example is Cystic fibrosis which is caused by a recessive allele. To have Cystic fibrosis, an individual need to have two copies of the faulty allele.
Sometimes, both alleles can be dominant. The condition where both alleles express equally is called codominance. Blood types are good examples of this condition. The blood group AB is the result of codominance of the A and B alleles.
According to a research from King’s College London, nearly 75 percent of immune traits are influenced by genes. The study adds to a developing body of evidence that our genetics significantly influence our immune system. The researchers, with the support of the NIHR Biomedical Research Centre at Guy’s and St Thomas’, analysed 23,000 immune characteristics in 497 adult female twins.
The researchers found that adaptive immune characteristics are mainly influenced by genetics. They also highlighted the importance of environmental factors such as diet, on determining the inmate immunity in adult life. The findings could result in a better understanding of the immune system and how it interacts with environmental factors. In addition, it could form the foundation of more research in a treatment of many diseases such as rheumatoid arthritis and psoriasis.
Dr Massimo Mansion, chief scientist from King’s College London said that adaptive immune responses appear to be more controlled by genome variations than he had previously thought. This means that people are likely to respond in an individualised way to an allergen or infection. This may have significant consequences for future personalised therapy.
Do you know people who are diligent about their health but still prone to gum diseases or tooth decay? It might not be their fault. Their condition may be linked to their genes.
According to scientists from the University Of Pittsburgh School Of Dental Medicine, certain genes variations are the cause of aggressive periodontitis and tooth decay. Dr. Alexandre Vieira, one of the researchers, said that the rate of dental caries is influenced by individual variations in a gene known as defensin 1 (DEFB1). This gene plays a major role in response against germs.
By analysing about 300 dental records and saliva samples from registry of the University of Pittsburgh School of Dental Medicine, the researchers gave each case a DMFT score (based on number of teeth that are missing, filled and decayed) and DMFS score (based on the number of teeth that missing, filled and decayed) Generally, people with fewer carriers boast of lower DMFT and DMFS scores. Also, the researcher found that all saliva samples had one of the three variants, dubbed C-44G, G-52A and G-20A, of and the DEFB1 gene.
The G-52A polymorphism was linked with lower DMFT scores. People with a G-20A copy had DMFS and DMFT scores that were five-times higher compared to individuals who had other variants.
No matter the effectiveness of a drug, it may not work for all people. Similarly, no matter how deadly a disease is, it can’t kill everyone that contracts it. The reason behind these facts is the same: each human being has different genetic makeup. Therefore, we need to address health issues based on each individual.
Among high-risk populations, researchers have discovered a small percentage of people who have shown either delayed development or resistance of AIDS. In 1996, a form of gene CCR5, a co-receptor, was found in high frequency in the HIV-resistant individuals. After detecting the gene, researchers were able to show that HIV virus required the co-receptor to enter and infect a T-cell. The deletion form of CCR5 known as CCR5-del32 cannot perform its usual functions, nor can it act as the co-receptor for the HIV. Therefore, people with a single copy of the CCR5-del32 allele are likely to experience delayed AIDS development while those with both copies of the CCR5-del32 allele do not develop AIDS.
When researchers studied the CCR5-del32 frequency in the general population, they discovered that the CCR5-del32 allele is seen in West Asian, European, and North African populations. Carrying a mutant CCR5-del32 allele also help fight infectious microorganisms such as Shigella and Salmonella.
Our brain, which is called the most complex thing in the universe, have 86 billion neurons with trillions of yet-unmapped connections. Understanding how the brain works is difficult problem which has afflicted the mankind for millennia. But this new study can offer the solution for the psychiatric disorders that made many people to suffer. To understand the brain, a roundworm, C elegans, is good model because it has only 302 neurons, which were completely mapped, with 6,000 connections. It looks like circuit board of biology. Although the brain has simple structure, it forms from simple reactions like searching for food and learning to avoid venom to complex reactions such as social behaviors.
The subject which says understanding this simple system will bring a development of understanding human brain was published on December 26, 2016, in Nature Methods.
Specifically, the idea of breadboards which help adding and correcting circuit elements in electrical and computer engineering is utilized in biology. In order to understand how the neural circuits in brains generate behavior, scientists need to control the activity of neurons as their needs. To do this, researchers have developed robust tools (transgenic actuators), that use drugs or light to activate or silence the neurons in which they are expressed.
Navin Pokala, Ph.D., assistant professor of Life Sciences at New York Institute of Technology (NYIT) College of Arts and Sciences, adapted the GAL4-UAS system for expressing transgenes in the nematode C elegans with researchers at Caltech university. This system, which uses a gene regulatory proteins from yeasts, greatly reduces the time and cost for making new cell-actuator combinations by simply mating already-constructed animals.
Pokala and his collaborators are planning to experiment variations of the GAL4-UAS system to control expression of actuator gene more precisely. Transgenic animal construction allows systematic change of the cells in the nervous system. It allows Pokala and colleagues to build a database linking neural perturbations to behaviors. As it combined with the previously mapped circuit wiring, this database will be a valuable resource for developing and testing models of nervous system function.