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Related Concept Videos

Cohesins02:20

Cohesins

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Cohesin protein complexes are a molecular glue that holds two sister chromatids together. They play an important role both in mitosis and meiosis. In mitosis, all cohesin complexes present on the chromosomes are removed before the start of the anaphase stage.
Cohesin complexes in Meiotic Division
Meiosis involves two distinct rounds of chromosomal segregation and cell divisions— Meiosis I followed by Meiosis II – producing four daughter cells. Meiosis I includes the separation of...
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Separation of Sister Chromatids02:17

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At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
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Differentiation of Common Myeloid Progenitor Cells01:15

Differentiation of Common Myeloid Progenitor Cells

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Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
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Anaphase Promoting Complex00:50

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The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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Condensins02:15

Condensins

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Condensins are large protein complexes that use ATP to fuel the assembly of chromosomes during mitosis. They transform the tangled, shapeless mass of post-interphase DNA into individualized chromosomes by compacting, organizing, and segregating chromosomal DNA.
The plant and animal cells contain two types of condensin complexes—condensin I and condensin II. Both complexes have five subunits: two SMC (Structural Maintenance of Chromosomes) subunits, a kleisin subunit, and two HEAT-repeat...
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Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Observing Mitotic Division and Dynamics in a Live Zebrafish Embryo
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Cohesin Mutations in Myeloid Malignancies.

Joseph B Fisher1, Maureen McNulty2, Michael J Burke3

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Mutations in the cohesin complex drive myeloid malignancies like Acute Myeloid Leukemia (AML) by enhancing stem cell self-renewal. These genetic alterations impact gene expression via chromatin changes, contributing to disease development.

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Area of Science:

  • Hematology
  • Cancer Genomics
  • Epigenetics

Background:

  • Acute Myeloid Leukemia (AML) is a serious blood cancer with poor outcomes.
  • Cohesin complex gene mutations are frequently found in myeloid malignancies.
  • These mutations are particularly common in Down syndrome-associated acute megakaryocytic leukemia (DS-AMKL).

Purpose of the Study:

  • To review the pathogenic mechanisms linking cohesin mutations to myeloid malignancies.
  • To elucidate how cohesin mutations confer enhanced self-renewal of hematopoietic stem and progenitor cells.
  • To discuss the role of cohesin mutations in gene expression alterations.

Main Methods:

  • Review of recent genome-wide sequencing studies.
  • Analysis of evidence linking cohesin mutations to chromatin accessibility.
  • Investigation of aberrant targeting of epigenetic complexes.

Main Results:

  • Cohesin mutations enhance self-renewal of hematopoietic stem and progenitor cells.
  • Evidence suggests alterations in chromatin accessibility due to cohesin mutations.
  • Aberrant targeting of epigenetic complexes is implicated in cohesin-mutated myeloid malignancies.

Conclusions:

  • Cohesin mutations are key drivers in the pathogenesis of myeloid malignancies.
  • Understanding these mechanisms is crucial for developing targeted therapies for AML and DS-AMKL.
  • Further research is needed to fully elucidate the complex interplay between cohesin, chromatin, and epigenetic regulation in these cancers.