F Rosa Rubicondior: Unintelligent Design - How a Cell Division Error Sometimes Causes Cancers - Incompetence or Malevolence?

Tuesday 14 May 2024

Unintelligent Design - How a Cell Division Error Sometimes Causes Cancers - Incompetence or Malevolence?

Two microscopy images of chromosomes. The left image shows chromosomes during mitosis (white). In orange, a centromere is visible consisting of two subdomains (arrows), each bound to a discrete bundle of microtubules (magenta). The right image depicts a dividing cancer cell showing a missegregating chromosome in the middle. The two centromere subdomains (arrows) of this chromosome appear split.

Credit: Carlos Sacristan Lopez. Copyright: Hubrecht Institute.
Research on centromere structure yields new insights.

Creationists, who, generally speaking, know little or nothing of biology and don't want to either because the risk of wondering it they could be wrong is far too great, are easily fooled by the frauds with a vested interest in keeping them simultaneously ignorant and imagining they have a deeper understanding than the millions of educated, working biomedical scientists who apply the Theory of Evolution every day of their working lives.

One thing they've been fooled into believing is that there is some sort of perfection in design inside a cell and that same designer is responsible for everything about living organisms.

But, in the last few years, under the onslaught of science, the frauds have needed to fall back from the demonstrably false notion of perfection of design in view if cancers, diseases and parasites, and now blame something for these obvious imperfections, which, by definition, could not be the products of a perfect designer god, do they have invented the biologically nonsensical notion of 'genetic entropy' and devolution caused by 'Sin' over which their omnipotent, omnibenevolent designer god is powerless.

And, again under the onslaught of science, the frauds have also conceded that evolution does indeed happen and happened at a massively accelerated rate to account for all the biodiversity produced by a small number of survivors of a genocidal flood just a few thousand years ago.

Describe the processes of mitosis and meiosis and how they can produce variance and errors, please. Mitosis and meiosis are both essential processes for cell division, but they occur in different contexts and produce different outcomes.

Mitosis is the process of cell division that occurs in somatic cells (non-reproductive cells) to produce two identical daughter cells, each with the same number of chromosomes as the parent cell. It consists of several stages: prophase, metaphase, anaphase, and telophase.

During prophase, the chromosomes condense and become visible. The nuclear envelope dissolves, and spindle fibers begin to form. In metaphase, the chromosomes align at the cell's equator. Then, in anaphase, the sister chromatids separate and move to opposite poles of the cell. Finally, in telophase, the chromosomes de-condense, and nuclear envelopes reform around the separated chromosomes, resulting in two identical daughter cells.

Meiosis is the process of cell division that occurs in germ cells (cells that give rise to gametes) to produce four non-identical daughter cells, each with half the number of chromosomes as the parent cell. Meiosis involves two rounds of division: meiosis I and meiosis II, each consisting of prophase, metaphase, anaphase, and telophase stages.

During meiosis I, homologous chromosomes pair up and exchange genetic material in a process called crossing over, increasing genetic diversity. Then, the homologous chromosomes separate, reducing the chromosome number by half. In meiosis II, similar to mitosis, sister chromatids separate, resulting in four haploid daughter cells.

Variance and Errors:
Both mitosis and meiosis can contribute to genetic variance, but meiosis plays a more significant role due to its involvement in sexual reproduction.
  1. Crossing Over (Recombination): In meiosis, crossing over occurs during prophase I, where homologous chromosomes exchange genetic material. This process shuffles alleles between homologous chromosomes, leading to genetic variation among the daughter cells.
  2. Independent Assortment: During metaphase I of meiosis, homologous chromosomes line up randomly at the cell equator, leading to the random distribution of maternal and paternal chromosomes into daughter cells. This independent assortment results in a vast number of possible combinations of chromosomes in the gametes, contributing to genetic diversity.
  3. Errors in Segregation: Errors during meiosis, such as nondisjunction, can lead to an incorrect distribution of chromosomes into daughter cells. Nondisjunction occurs when chromosomes fail to separate properly during meiosis I or meiosis II, leading to aneuploidy (an abnormal number of chromosomes) in the resulting gametes. For example, Down syndrome (trisomy 21) results from an extra copy of chromosome 21 due to nondisjunction during meiosis.
  4. Mutations: Both mitosis and meiosis can also be prone to errors due to mutations, which are changes in the DNA sequence. These mutations can occur spontaneously or due to external factors such as radiation or chemical exposure. If mutations occur in germ cells during meiosis, they can be passed on to offspring, potentially leading to genetic disorders or variations.
But, evolution, whether at the warp speed creationists now claim, or under the normal processes that biological science has identified depends first and foremost on variance - in other words, when an organism reproduces, there are occasional errors that produce the small differences that are then assorted by environmental selectors so deleterious ones are quickly eliminated and advantageous ones spread throughout the species gene pool.

But hang on! Creationists proponents of 'genetic entropy' and 'devolution' claim the initial creation was perfect! So how can there have been variance? A perfect creation, replicating perfectly, could not have produced variations on which natural selection can act!

So, the fact of variance - on which creationists' accepted warp speed evolution depends - proves the initial creation could not have been perfect!

But of course, it never was perfect and no-one who understands the fundamentals of biology would ever claim it was. The fact is, the cell-replication process, whether it for growth, repair or replacement of worn-out cells in a multicellular organism, or to produce the male and female gametes for sexual reproduction, is subject to frequent error because the process of replicating the DNA is error prone. In multicellular animals, these are so frequent that a repair mechanism has also evolved, which itself doesn't always work to repair all the errors.

There is no sign of perfect design to be seen anywhere in the process.

Or if there is, there are only two ways of regarding the designer - incompetent in the extreme, or malevolent in the extreme; the latter especially so since creationists insist that it is also omniscience, so knew exactly what its creation would do, including the results of the errors, and designed it that way deliberately.

And one of the things imperfect replication causes is cancer when errors in reproducing the genome in two daughter cells causes a cell to begin to replicate its genome and go into uncontrolled cycles of replication. Cells that bud off from the resulting tumour can lodge in various parts of the body and set up a new tumour there. And, to make matters worse, these cancer cells can evolve in response to the drugs given to kill them, like bacteria evolving resistance to antibiotics, so a few surviving cells can start a new colony that is now resistant to the anti-cancer drugs.

One of the reasons this goes wrong was discovered recently by a team of researchers from the Kops group from the Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences, Utrecht, Netherlands in collaboration with researchers from the University of Edinburgh.
The Hubrecht Institute is a research institute of the Royal Netherlands Academy of Arts and Sciences (KNAW), situated on the Utrecht Science Park. Since 2008, the Hubrecht is affiliated with the UMC Utrecht. This allowed the institute to grow into an internationally renowned research institute and facilitated the link with (pre)clinical research. The Hubrecht Institute has a partnership with the European Molecular Biology Laboratory (EMBL) based on shared institutional goals, scientific synergy and complementarity.

The problem begins with a badly designed centromere which is composed of two parts which need to coordinate their actions, but sometime fail to do so. The centromere is the segment of a chromosome where spindle fibres are attached to pull the duplicated chromosomes apart, so they end up in each of the two daughter cells. If these spindles are not properly attached, the separation can fail.

The findings of the team of researchers are the subject of an open access paper in Cell and is explained in a news release from the Hubrecht Institute:
Research on centromere structure yields new insights into the mechanisms of chromosome segregation errors

Researchers from the Kops group, in collaboration with researchers from the University of Edinburgh, made a surprising new discovery in the structure of the centromere, a structure that is involved in ensuring that chromosomes are segregated properly when a cell divides. Mistakes in chromosome segregation can lead to cell death and cancer development. The researchers discovered that the centromere consists of two subdomains. This fundamental finding has important implications for the process of chromosome segregation and provides new mechanisms underlying erroneous divisions in cancer cells. The research was published in Cell on May 13th 2024.

Our bodies consist of trillions of cells, most of which have a limited life span and therefore need to reproduce to replace the old ones. This reproduction process is referred to as cell division or mitosis. During mitosis, the parent cell will duplicate its chromosomes in order to pass down the genetic material to the daughter cells. The resulting identical pairs of chromosomes, the sister chromatids, are held together by a structure called the centromere. The sister chromatids then need to be evenly split over the two daughter cells to ensure that each daughter cell is an exact copy of the parent cell. If errors happen during the segregation, one daughter cell will have too many chromosomes, while the other has too few. This can lead to cell death or cancer development.

The role of the centromere
The centromere is a part of the chromosome that plays a vital role in chromosome segregation during mitosis. The process of dividing the sister chromatids over the cells is guided by the interaction between the centromeres and structures known as spindle microtubules. These spindle microtubules are responsible for pulling the chromatids apart and thus separating the two sister chromatids. Carlos Sacristan Lopez, the first author of this study, explains: ‘If the attachment of the centromere to the spindle microtubules does not occur properly it leads to chromosome segregation mistakes which are frequently observed in cancer.’ Understanding the structure of the centromere can contribute to more insights into the function of the centromere and its role in erroneous chromosomal segregation.

A surprising discovery
To investigate the centromere structure, the researchers used a combination of imaging and sequencing techniques. The super-resolution microscopy imaging took place at the Hubrecht Institute, while the group of Bill Earnshaw performed the sequencing. This collaboration led to a surprising new discovery in the centromere structure. Previously believed to consist of a compact structure attaching to multiple spindle microtubules, it was instead revealed that the centromere consists of two subdomains. Carlos explains: ‘This discovery was very surprising, as subdomains bind microtubules independently of each other. Yet, to form correct attachments, they must remain closely connected. In cancer cells, however, we often observe that subdomains uncouple, resulting in erroneous attachments and chromosome segregation errors.’
Two microscopy images of chromosomes. The left image shows chromosomes during mitosis (white). In orange, a centromere is visible consisting of two subdomains (arrows), each bound to a discrete bundle of microtubules (magenta). The right image depicts a dividing cancer cell showing a missegregating chromosome in the middle. The two centromere subdomains (arrows) of this chromosome appear split.

Credit: Carlos Sacristan Lopez. Copyright: Hubrecht Institute.
This very exciting and fundamental discovery contributes to our understanding of the origin of chromosome segregation errors which are frequently seen in cancer.
  • Core centromere chromatin reorganizes into a two-domain structure in mitosis
  • Each centromere subdomain engages a discrete microtubule bundle
  • Lagging chromosomes in cancer cells have subdomains bound to opposite spindle poles
  • Cohesin stabilizes centromere subdomains to avoid formation of merotelic attachments

Centromeres are scaffolds for the assembly of kinetochores that ensure chromosome segregation during cell division. How vertebrate centromeres obtain a three-dimensional structure to accomplish their primary function is unclear. Using super-resolution imaging, capture-C, and polymer modeling, we show that vertebrate centromeres are partitioned by condensins into two subdomains during mitosis. The bipartite structure is found in human, mouse, and chicken cells and is therefore a fundamental feature of vertebrate centromeres. Super-resolution imaging and electron tomography reveal that bipartite centromeres assemble bipartite kinetochores, with each subdomain binding a distinct microtubule bundle. Cohesin links the centromere subdomains, limiting their separation in response to spindle forces and avoiding merotelic kinetochore-spindle attachments. Lagging chromosomes during cancer cell divisions frequently have merotelic attachments in which the centromere subdomains are separated and bioriented. Our work reveals a fundamental aspect of vertebrate centromere biology with implications for understanding the mechanisms that guarantee faithful chromosome segregation.

Graphical abstract

During cell division, spindle microtubules attach to chromosomes at centromeres, specialized regions responsible for kinetochore assembly and epigenetically defined by the histone H3 variant CENP-A.1,2 Vertebrate chromosomes have “regional” centromeres, which are usually enriched for high-copy number tandemly repeated satellite sequences associated into domains known as higher order repeats (HORs).1,2,3 Satellite repeats, however, are not essential for centromere formation, as evolutionarily new centromeres occupy non-repetitive regions in several species, including chickens and equines,4,5,6,7 and neocentromeres are observed in humans in rare cases.1,2,8

The CENP-A-enriched core centromere associates with the constitutive centromere-associated network (CCAN) to build the kinetochore1 and is flanked by pericentromeres rich in methylated DNA and lacking CENP-A. CENP-A nucleosomes in the core centromere are interspersed with canonical histone H3-containing nucleosomes.9 CENP-A nucleosomes of the core centromere pack into an as-yet unknown higher-order organization.2,3,10 Current models assume that centromeric chromatin scaffolds a compact kinetochore structure that binds a single bundle of microtubules (the kinetochore fiber, or k-fiber) in mitosis.3,9,11,12 This organization is thought to provide rigidity to the kinetochore, allowing biorientation and promoting faithful chromosome segregation.

The structural maintenance of chromosomes (SMCs) family of proteins are essential drivers of the three-dimensional (3D) chromatin organization13,14 and important regulators of centromeres. Pericentromeric cohesin keeps sister chromatids tethered during cell division,13,14,15 while condensin provides stiffness to the (peri)centromere.16,17,18 Both are required to prevent the formation of merotelic attachments.19,20,21,22 Although the role of SMC complexes in compaction of regional centromeres remains largely speculative, important insights have been obtained by studying the point centromere of Saccharomyces cerevisiae, with its single CENP-A nucleosome. In S. cerevisiae, cohesin and condensin occupy distinct subdomains of the pericentromere.23,24 In one recent model, the pericentromere forms a bottlebrush consisting of arrays of loops cross-linked by cohesin, which is responsible both for keeping sister chromatids together and for cross-linking the arrays of loops extruded by condensin.25,26 The cross-linked loops enable centromeres to resist spindle forces.

Here we investigated the higher-order organization of regional vertebrate centromeres and its functional consequences on kinetochore formation, spindle assembly, and chromosome segregation.

Figure 1. Subdomain organization of the vertebrate regional centromere
(A–C) ExM (CENP-A, DAPI) of a metaphase RPE-1 cell. Arrowheads in inset: CENP-A subdomains.
(B) Blow-ups of the dotted boxes in (A).
(C) Line intensity profiles across centromere subdomains in (B). Distance between peaks is indicated.
(D) Fraction of centromeres per cell with the indicated number of CENP-A subdomains. Complex: centromeres with >4 subunits or heterogenoeus shapes (mean ± SD of 4 independent experiments; n = 21 cells, 829 centromeres).
(E) Distance between CENP-A subdomains in bipartite centromeres in ExM images (mean ± SD of 3 independent experiments, n = 240 centromeres). Large dots, independent experiments; small dots, single centromeres.
(F) CENP-C immunostaining in stretched chromosomes. Arrowheads: CENP-C subdomains.
(G) (Left) ExM image of CENP-A and CENP-B in PDNC4 cells with neocentromere in chromosome 4 (Neo4q21.3).8 (Right) Blow-up of the box in (G). Neo4q21.3 is recognized by the lack of CENP-B signal between sister centromeres; alphoid cen: a canonical centromere containing α-satellite repeats. Arrowheads: CENP-A subdomains.
(H) ExM (ACA, anti-centromere antibody) of mouse embryonic fibroblast (MEF). Arrowheads: ACA subdomains. See also Figure S1J.
(I) ExM (CENP-T) of a chicken DT40 cell. Arrowheads: CENP-T subdomains.
(J) Cartoon depicting core centromere organization. Two subdomains (orange balls) are each associated to one chromosome arm. In all figures, NI, normalized intensity; Z, plane of z stack or maximum intensity projection of indicated planes.
See also Figure S1.

Figure S1. Subdomain organization of the regional centromere of vertebrates, related to Figure 1
(A) 3D reconstructions of the centromeres shown in Figures 1A and 1B.
(B–D) Representative ExM image of CENP-A in RPE-1 cells in metaphase (B). Blow-ups, centromeres enclosed in the boxes (C), and line intensity profiles across centromere subdomains (D). The distance between peaks is indicated.
(E) Examples of tetrapartite centromeres. Asterisks: small subdomains; arrowheads: main two subdomains.
(F and G) Immunostaining of CENP-A in HCT-116 cells imaged by confocal and STED microscopy. Numbered squares enclose the same centromeres in both conditions. Line intensity profiles across centromere subdomains (G). The distance between peaks is indicated.
(H and I) iSIM live-cell imaging (lateral resolution ⁓125 nm) of a U2OS cell expressing mCherry-CENP-A and H2B-mNeon (H). Blow-ups of the orange box and other regions are shown on the right. Line intensity profiles across centromere subdomains (I). The distance between peaks is indicated.
(J) Representative ExM image of a mouse embryonic fibroblast (MEF) immunostained with ACA (anti-centromere antibody). Arrowheads: ACA subdomains. The image belongs to the same cell shown in Figure 1H. Z specifies the plane of the z stack. NI, normalized intensity.
Sacristan, Carlos; Samejima, Kumiko; Ruiz, Lorena Andrade, et al;
Vertebrate centromeres in mitosis are functionally bipartite structures stabilized by cohesin Cell (2024) 10.1016/j.cell.2024.04.014

Copyright: © 2024 The authors.
Published by Elsevier. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
So, given that any evolution would be impossible if the original genome was created perfectly, because there could be no variation produced on which natural selection could work, as explained above, creationists can't logically blame 'genetic entropy' and 'devolution' caused by 'Sin', which leaves them with just three possibilities for this cancer-causing design error: incompetence; malevolence or evolution.

I wonder which one they'll go for.


The Unintelligent Designer: Refuting The Intelligent Design Hoax

ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.

Available in Hardcover, Paperback or ebook for Kindle


The Malevolent Designer: Why Nature's God is Not Good

This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

Illustrated by Catherine Webber-Hounslow.

Available in Hardcover, Paperback or ebook for Kindle


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1 comment :

  1. The creator is both incompetent and malevolent and let's not forget He is insane as well. Mentally blind and morally blind. A cosmic Dr. Jekyll and Mr Hyde. Amoral non moral. No conscience.
    How can any thinking person believe that the creation was originally perfect? That's so far from reality. It never was perfect and never will be. If something sounds too good to be true it usually is. The creator doesn't have the intelligence and doesn't have kindness and doesn't have the ability to make a perfect creation. The creator doesn't have the sense to make a perfect creation. The creation is far far from perfect and in fact is extremely flawed in so many ways. It's a huge embarrassment for creationists.
    And the false myth of Adam and Eve's Original Sin continues to be preached by creationists. Come on Creationists. The belief that Adam and Eve eating a forbidden apple caused all Human evil and sin and caused all Natural evil is the height of ignorance and the height of delusion. It's false science, false history, false reality. The idea that the entire creation was spoiled and ruined just because two primitive humans ate a forbidden apple is unbelievable. This absurd false myth needs to be refuted. Creationists choose to believe in false myths.


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