Cloning, a topic that has captured the imagination of many, continues to be a subject of scientific interest, ethical debates, and speculative musings. While its various forms and implications have been widely discussed, this article aims to provide an overview of cloning, present examples of successful cloning in different organisms, explore the mechanisms involved, and address the reports and speculations surrounding possible human cloning.

Understanding Cloning: Cloning is the process of creating an organism that is genetically identical to another individual. It can occur naturally, such as with identical twins, or it can be achieved artificially through scientific techniques. Artificial cloning techniques include somatic cell nuclear transfer (SCNT), where the nucleus of a donor cell is transferred into an enucleated egg cell, and reproductive cloning, which aims to create a living copy of an existing organism.

Scientists have discovered how our DNA can use a genetic fast-forward button to make new genes for quick adaptation to our ever-changing environments.

During an investigation into DNA replication errors, researchers from Finland’s University of Helsinki found that certain single mutations produce palindromes, which read the same backward and forward. Under the right circumstances, these can evolve into microRNA (miRNA) genes.

These tiny, simple genes play a significant role in regulating other genes. Many miRNA genes have been around for a long time in evolutionary history, but scientists discovered that in some animal groups, like primates, brand-new miRNA genes suddenly appear.

FDA approval for revolutionary Sickle Cell Disease gene-editing treatment promises a bright future.

As Vertex and CRISPR Therapeutics’ exa-cel and Verve Therapeutics’ VERVE-101 move forward, questions remain about possible drawbacks of such therapies.

Many Black Americans who are thought to have a high risk of developing kidney disease possess a protective genetic variant that nullifies the extra risk, a new study from Columbia researchers has found. The work is published in the journal Nature Communications.

The study found that high-risk people who carry this variant have a risk of developing kidney disease much closer to that of the general population.

The findings will have an immediate impact on clinical practice, says study leader Simone Sanna-Cherchi, MD, associate professor of medicine at Columbia’s Vagelos College of Physicians and Surgeons.

Researchers at the Francis Crick Institute, UCL, and MSD have identified a potential treatment target for a genetic type of epilepsy.

Developmental and epileptic encephalopathies are rare types of epilepsy that start in early childhood. One of the most common types of genetic epilepsy, CDKL5 deficiency disorder (CDD), causes seizures and impaired development. Children are currently treated with generic antiepileptic drugs, as there aren’t yet any disease-targeting medications for this disorder.

CDD involves losing the function of a gene producing the CDKL5 enzyme, which phosphorylates proteins, meaning it adds an extra phosphate molecule to alter their function. Until now, researchers have not been sure how genetic mutations in CDKL5 cause CDD.