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1. How Dantu Blood Group protects against malaria—and how all humans could benefit
In 2017, researchers discovered that the rare Dantu blood variant, which is found regularly only in parts of East Africa, provides some degree of protection against severe malaria.
The secret of how the Dantu genetic blood variant helps to protect against malaria has been revealed for the first time by scientists now.
They found that red blood cells in people with the rare Dantu blood variant have a higher surface tension that prevents them from being invaded by the world's deadliest malaria parasite, Plasmodium falciparum.
Analysis of the characteristics of the red blood cell samples indicated that the Dantu variant created cells with a higher surface tension—like a drum with a tighter skin. At a certain tension, malaria parasites ‘re no longer able to enter the cell, halting their lifecycle and preventing their ability to multiply in the blood. The Dantu blood group has a novel 'chimeric' protein that is expressed on the surface of red blood cells, and alters the balance of other surface proteins.
This finding could also be significant in the wider battle against malaria. Because the surface tension of human red blood cells increases as they age, it may be possible to design drugs that imitate this natural process to prevent malaria infection or reduce its severity.
2. New finding: A lack of oxygen in tumours promotes metastasis
Metastases are formed by cancer cells that break away from the primary tumour. A research group has now identified lack of oxygen as the trigger for this process. The results reveal an important relationship between the oxygen supply to tumours and the formation of metastases. This research may open up new treatment strategies for cancer.
The chances of recovery significantly worsen when a tumour metastasizes. Previous research has shown that metastases are formed by clusters of cancer cells that separate from the primary tumour and migrate to new tissue through the bloodstream. However, thus far little has been known about why these clusters of circulating tumour cells (CTCs) leave the tumour in the first place.
It has been shown now that a lack of oxygen is responsible for the separation of CTC clusters from the tumour. This is an important starting point for the development of new cancer treatments.
Different areas of a tumour are supplied with different levels of oxygen: cancer cells with a lack of oxygen were found wherever the tumour had comparatively fewer blood vessels—in the core of the tumour as well as in clearly defined peripheral areas. Next, the research team investigated the CTC clusters that had separated from these tumours and found that they similarly suffered from a lack of oxygen. This led to the conclusion that cells leave the tumour if they do not receive enough oxygen.
Source: Cell Reports (2020). DOI: 10.1016/j.celrep.2020.108105
3. The control mechanism that allows cells to form tissues and anatomical structures in the developing embryo identified
The first few hours of every multicellular organism's life seem incongruously chaotic. After fertilization, a once tranquil single-celled egg divides again and again, quickly becoming a visually tumultuous mosh pit of cells jockeying for position inside the rapidly growing embryo. Amid this apparent pandemonium, cells begin to self-organize. Soon, spatial patterns emerge, serving as the foundation for the construction of tissues, organs and elaborate anatomical structures from brains to toes and everything in between.
How do these specific patterns arise in cells and how to they form tissues?
Now researchers have discovered a key control mechanism that cells use to self-organize in early embryonic development.
Studying spinal cord formation in zebrafish embryos, a team revealed that different cell types express unique combinations of adhesion molecules in order to self-sort during morphogenesis. These "adhesion codes" determine which cells prefer to stay connected, and how strongly they do so, even as widespread cellular rearrangements occur in the developing embryo.
The researchers found that adhesion codes are regulated by morphogens, master signaling molecules long known to govern cell fate and pattern formation in development. The results suggest that the interplay of morphogens and adhesion properties allows cells to organize with the precision and consistency required to construct an organism.
These insights into how cells self-organize in early development could also aid efforts to engineer tissues and organs for clinical uses such as transplantation.
"An adhesion code ensures robust pattern formation during tissue morphogenesis" Science (2020). science.sciencemag.org/lookup/ … 1126/science.aba6637
4. Scientists discovered a missing gene fragment that's shedding new light on how males develop
It's one of the most important genes in biology: Sry, the gene that makes males male. Development of the sexes is a crucial step in sexual reproduction and is essential for the survival of almost all animal species. Researchers report the surprise discovery of an entirely new part of the Sry gene in mice—a part we had no idea existed.
Scientists discovered Sry in 1990. It is the gene on the Y (male) chromosome that leads to the development of male characteristics in mice, humans and most other mammals. Since then, Sry has been the subject of intense study worldwide because of its fundamental role in mammalian biology.
We have come to understand, in some detail, how Sry acts to trigger a cascade of gene activity that results in the formation of testes, instead of ovaries, in the embryo. Testes then stimulate the formation of other male characteristics.
Researchers have understood the Sry gene is made up of one exon, a segment of a gene used to code for amino acids, the building blocks of proteins. This can be compared to a computer file consisting of one contiguous block of data on a hard disk.
The newest research reveals there's actually a second exon in mouse Sry. This is like finding a whole new separate block of previously hidden data. New sequencing approaches revealed what appeared to be two versions of Sry: a short, single-exon form and a longer, two-exon form. Scientists called this two-exon version "Sry-T."
They removed the new exon using CRISPR, a gene editing tool that lets researchers alter DNA precisely and discovered this prevented Sry from functioning: XY mice (which would normally develop as males) developed as females instead.
Conversely, adding Sry-T to fertilized XX mouse eggs (which would normally develop as females) resulted in males.
The mouse Sry locus harbors a cryptic exon that is essential for male sex determination, Science 02 Oct 2020: Vol. 370, Issue 6512, pp. 121-124 ,