Answer:
1. Chromatin condense into chromosomes.
4. Homologous chromosomes pair up (formation of tetrads).
5. Homologous chromosomes separate and move to poles.
2. Sister chromatids separate.
3. Chromosomes unravel in to chromatin.
Explanation:
This question portrays the process of meiosis in a cell. The ordered sequence of events in the options are:
1. Chromatin condense into chromosomes - This process occurs in the Prophase stage. Prior to the cell division, the nuclear material is found as Chromatin material. This Chromatin material then undergoes condensation to form visible chromosomes.
4. Homologous chromosomes pair up (formation of tetrads) - This process also occurs during the Prophase stage of meiosis I. In this stage, homologous chromosomes (similar but non-identical chromosomes received from each parent) are paired up side by side to form a structure known as TETRAD or BIVALENT.
5. Homologous chromosomes separate and move to poles - This process characterizes the Anaphase stage of meiosis I. Homologous chromosomes are pulled apart to opposite poles of the cell by spindle microtubules.
2. Sister chromatids separate - After meiosis I, meiosis II involving sister chromatids instead of homologous chromosomes follows. In the Anaphase stage of meiosis II specifically, sister chromatids are pulled apart towards opposite poles of the cell.
3. Chromosomes unravel in to chromatin - After the whole division process i.e. karyokinesis (division of the nuclear material), the chromosomes begin to unravel to form the CHROMATIN threads once again. This process occurs in the Telophase stage of meiosis.
Decomposers get energy from dead or decaying matter. Examples are fungi, bacteria, some insects and snails.
Protein-protein interactions within the CARMA1-BCL10-MALT1 complex:
- The T-cell receptor and B-cell receptor-dependent NF-B induction and lymphocyte activation are mediated by the CBM complex, which is made up of the proteins CARMA1, BCL10, and MALT1.
- Each of the proto-oncoproteins CARMA1, BCL10, and MALT1 is a somatic gain-of-function mutation or chromosomal translocation, and dysregulation of CBM signaling is a characteristic of numerous lymphoid malignancies, including Activated B-cell Diffuse Large B-cell Lymphoma.
- Moreover, a number of immunological dysregulation diseases have been linked to both gain- and loss-of-function germline mutations in CBM complex proteins.
- Over the past ten years, careful examination of the interactions of CBM components has yielded a wealth of detailed structural knowledge.
- Here, we discuss important discoveries about the molecular nature of these protein-protein interactions that have helped the research develop a detailed understanding of how these proteins come together to form high-order filamentous CBM complexes.
- Approaches to therapeutic suppression of the CBM complex have thus far centered on obstructing MALT1 protease activity in order to treat lymphoid malignancy and/or autoimmunity.
- The structural effects of MALT1 protease inhibitors on significant protein-protein interactions are also reviewed in detail.
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Veins don’t always conduct oxygen poor blood. The pulmonary vein brings reoxygenated blood from the lungs into the heart