When the motor is not pulling

Why do eggs get confused in chromosomes

Kirill Stasevich, Science and Life (nkj.ru )

During fertilization, the genomes of the father and mother are combined: the chromosomes from the mother sit in the egg, the chromosomes from the father sit in the sperm. At the same time, both in the egg and in the sperm, the set of chromosomes is single, and in all other cells of the body it is double. When germ cells are formed, their progenitor cells divide in a special way - so that only one chromosome set remains in the mature egg and sperm, that is, each chromosome should be in only one copy. If something goes wrong, if an extra chromosome remains in the germ cell, or, conversely, some chromosome is suddenly missing, everything ends badly: the embryo will develop with abnormalities, a miscarriage may occur, and if the child is still born, he will have some kind of malformation. (The most famous example is Down syndrome, when the twenty—first chromosome turns out to be in triplicate.)

At the same time, it is known that it is human eggs that are particularly prone to chromosomal errors, and it is even known at what stage they occur. When a cell divides, a so—called division spindle is formed in it - a complex apparatus of protein strands that go from two opposite poles of the cell to its middle, where tightly packed chromosomes are lined up.

Protein filaments (called microtubules) attach to chromosomes and begin to drag them to the poles. It is important that only one copy of each chromosome goes to each pole. Errors can occur for various reasons: for example, microtubules have not attached to any chromosome at all. It may be otherwise: in some chromosome, both copies have gone to one half, because in a dividing cell, not two pole points have formed, from which protein strands come out, but more. That is, on one half of the cell there is one pole of microtubules, and on the other — two.

Staff of the Institute of Interdisciplinary Research Max Planck Societies write in Science (So et al., Mechanism of spindle pole organization and instability in human oocytes) that the reason for this splitting of poles is a lack of KIFC1 protein in eggs, and in human eggs it is not enough by default. The researchers compared human oocytes (precursors of mature eggs) with the eggs of mice, pigs and cows. In animals, the level of KIFC1 protein was higher than in humans, and if its number was artificially lowered in animal oocytes, then "pole splitting" began in oocytes and, as a result, errors appeared in the distribution of chromosomes between daughter cells. (The oocytes that were used in the experiments had to be shared again to get a mature egg ready for fertilization.)

KIFC1 is a motor protein that interacts with protein strands stretching to chromosomes, pulling them into a bundle. By not allowing microtubules to run apart, KIFC1 thereby prevents the formation of extra poles of attraction of chromosomes, controls the number of microtubules and their behavior. If it is artificially added to human oocytes, there will be fewer chromosomal errors, and, probably, you can even figure out how to increase it in those oocytes that are in the ovaries. It is hardly worth raising it in all women, but at least KIFC1 could solve problems with permanent miscarriages that occur due to improper chromosome distribution, or protect the child from congenital developmental abnormalities during in vitro fertilization.

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