Lifeboat Foundation

As sponges and ctenophores are such disparate animals¹³, the nature of the first diverging animal lineage has implications for the evolution of fundamental animal characteristics. Adult sponges are generally sessile filter-feeding organisms with body plans organized into reticulated water-filtration channels, structures built out of silica or calcium carbonate, and specialized cell types and tissues used for feeding, reproduction and self-defence, but they lack neuronal and muscle cells¹⁵. By contrast, ctenophores are gelatinous marine predators that move using eight longitudinal ‘comb rows’ of ciliary bundles^16,17; they are superficially similar but unrelated to cnidarian medusae^13,18 and possess multiple nerve nets¹⁹. Thus, whereas the sponge-sister scenario suggests a single origin of neurons on the ctenophore–parahoxozoan stem, the ctenophore-sister scenario implies either that either ancestral metazoan neurons were lost in the sponge lineage, or that there was convergent evolution of neurons in the ctenophore and parahoxozoan lineages^3,6. Similar considerations apply to other metazoan cell types¹⁸, gene regulatory networks, animal development^13,18 and other uniquely metazoan features.

Despite its importance for understanding animal evolution, the relative branching order of sponges, ctenophores and other animals has proven to be difficult to resolve². The fossil record is largely silent on this issue as verified Precambrian sponge fossils are extremely rare²⁰ and putative fossils of the soft-bodied ctenophores are difficult to interpret²¹. Morphological characters of living groups (for example, choanocytes of sponges) are not sufficient to resolve the question because true homology is difficult to assign, and such characters are easily lost or can arise convergently^13,22. The ctenophore-sister hypothesis is supported by a pair of gene duplications shared by sponges, bilaterians, placozoans and cnidarians but not ctenophores²³. Although sophisticated methods for sequence-based phylogenomics have been developed and applied to increasingly large molecular datasets, there is still considerable debate about the relative position of sponges and ctenophores as results are sensitive to how sequence evolution is modelled¹¹, which taxa or sites are included^24,25, and the effects of long-branch artifacts and nucleotide compositional variation²⁶. New approaches are needed.

We reasoned that patterns of synteny, classically defined as chromosomal gene linkage without regard to gene order²⁷, could provide a powerful tool for resolving the ctenophore-sister versus sponge-sister debate. Chromosomal patterns of gene linkage evolve slowly in many lineages^12,28,29,30, probably because it is improbable for interchromosomal translocations to be fixed in populations with large effective population sizes^28,31,32. Notably, some changes in synteny are effectively irreversible. For example, when two distinct ancestral synteny groups are combined onto a single chromosome by translocation, and subsequent intrachromosomal rearrangements mix these two groups of genes, it is very unlikely that the ancestral separated pattern will be restored by further rearrangement and fission, in the same sense that spontaneous reduction in entropy is improbable¹². Such rare and irreversible changes are particularly useful for resolving challenging phylogenetic questions as they give rise to shared derived features that unambiguously unite all descendant lineages^33,34,35. Deeply conserved syntenies observed between animals and their closest unicellular relatives¹² suggest that outgroup comparisons could be used to infer ancestral metazoan states and polarize changes within animals to address the sponge-sister versus ctenophore-sister debate. Yet, chromosome-scale genome sequences of the unicellular or colonial eukaryotic outgroups closest to animals (choanoflagellates, filastereans and ichthyosporeans) have not been reported.

For more than a century, biologists have wondered what the earliest animals were like when they first arose in the ancient oceans more than half a billion years ago.

Searching among today’s most primitive-looking animals for the earliest branch of the animal tree of life, scientists gradually narrowed the possibilities down to two groups: sponges, which spend their entire adult lives in one spot, filtering food from seawater; and comb jellies, voracious predators that oar their way through the world’s oceans in search of food.

In a new study published this week in the journal Nature, researchers use a novel approach based on chromosome structure to come up with a definitive answer: Comb jellies, or ctenophores (pronounced teen’-a-fores), were the first lineage to branch off from the animal tree. Sponges were next, followed by the diversification of all other animals, including the lineage leading to humans.

A new study adds to an emerging, radically new picture of how bacterial cells continually repair faulty sections of their DNA.

Published online May 16 in the journal Cell, the report describes the molecular mechanism behind a DNA repair pathway that counters the mistaken inclusion of a certain type of molecular building block, ribonucleotides, into genetic codes. Such mistakes are frequent in code-copying process in bacteria and other organisms. Given that ribonucleotide misincorporation can result in detrimental DNA code changes (mutations) and DNA breaks, all organisms have evolved to have a DNA repair pathway called ribonucleotide excision repair (RER) that quickly fixes such errors.

Last year a team led by Evgeny Nudler, Ph.D., the Julie Wilson Anderson Professor in the Department of Biochemistry and Molecular Pharmacology at NYU Langone Health, published two analyses of DNA repair in living E. coli cells. They found that most of the repair of certain types of DNA damage (bulky lesions), such as those caused by UV irradiation, can occur because damaged code sections have first been identified by a protein machine called RNA polymerase. RNA polymerase motors down the DNA chain, reading the code of DNA “letters” as it transcribes instructions into RNA molecules, which then direct protein building.

NewLimit, a company working towards the radical extension of human healthspan using epigenetic reprogramming has announced it has secured $40 million in Series A funding from prominent investors including Dimension, Founders Fund, and Kleiner Perkins.

This investment further bolsters the company’s belief that therapies to delay, halt or even reverse aging can be found through the exploration of epigenetic reprogramming. With a strong belief that their innovative approach can also address various age-related diseases, NewLimit aims to revolutionize the field of aging biology and pave the way for transformative advancements in healthcare.

Longevity. Technology: Epigenetic reprogramming is an emerging but exciting field of geroscience. It involves the identification of specific sets of transcription factors that can induce changes in gene expression and cellular behavior, effectively reversing or modifying the epigenetic markers associated with aging. This approach offers a unique opportunity to rejuvenate cells and tissues, potentially slowing down or even reversing the effects of aging and its related diseases. NewLimit says that while its products are designed to treat aging itself, the company also believes “these products could treat or prevent many diseases associated with aging, including fibrosis, infectious disease, and neurodegenerative disease.”

Scientists with the Human Pangenome Reference Consortium have made groundbreaking progress in characterizing the fraction of human DNA that varies between individuals. They have assembled genomic sequences of 47 people from around the world into a so-called pangenome in which more than 99 percent of each sequence is rendered with high accuracy.

For two decades, scientists have relied on the human reference genome as a standard to compare against other genetic data. Thanks to this reference genome, it was possible to identify genes implicated in specific diseases and trace the evolution of human traits, among other things.

However, it has always been a flawed tool: 70% of its data came from a single man of predominantly African-European background whose DNA was sequenced during the Human Genome Project. Hence, it can reveal very little about individuals on this planet who are different from each other, creating an inherent bias in biomedical data believed to be responsible for some of the health disparities affecting patients today.

In a major advance, scientists have assembled genomic sequences of 47 people from diverse backgrounds to create a pangenome, which offers a more accurate representation of human genetic diversity than the existing reference genome. This new pangenome will help researchers refine their understanding of the link between genes and diseases, and could ultimately help address health disparities.

For more than 20 years, scientists have relied on the human reference genome, a consensus genetic sequence, as a standard against which to compare other genetic data. Used in countless studies, the reference genome has made it possible to identify genes implicated in specific diseases and trace the evolution of human traits, among other things.

But it has always been a flawed tool. One of its biggest problems is that about 70 percent of its data came from a single man of predominantly African-European background whose DNA.

Eight years after the technology was approved by government authorities, it can be reported that at least one child with DNA from three different people has been born to parents in the United Kingdom.

The announcement isn’t exactly ‘new’ knowledge, but reporters at The Guardian were able to prompt an official confirmation with a freedom of information request.

The University of Newcastle in collaboration with the Newcastle Fertility Center are pioneers in what is known as mitochondrial replacement therapy (MRT), a special form of in vitro fertilization (IVF) designed to prevent severe genetic diseases in future babies.

A new study in Nature hunted down another piece to the aging puzzle. In five species across the evolutionary scale—worms, flies, mice, rats, and humans—the team honed in on a critical molecular process that powers every single cell inside the body and degrades with age.

The process, called transcription, is the first step in turning our genetic material into proteins. Here, DNA letters are reworked into a “messenger” called RNA, which then shuttles the information to other parts of the cell to make proteins.

Scientists have long suspected that transcription may go awry with aging, but the new study offers proof that it doesn’t—with a twist. In all five of the species tested, as the organism grew older the process surprisingly sped up. But like trying to type faster when blindfolded, error rates also shot up.

Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhD

Discount Links:
NAD+ Quantification: https://www.jinfiniti.com/intracellular-nad-test/
Use Code: ConquerAging At Checkout.

Continue reading “Vitamin B6: Did It Increase NAD? (Test Results)” »