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the claim
Most mutations originate during mitosis rather than meiosis
the verdict
INSUFFICIENT LEANING
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the weight of evidence
4 sources for · 0 against

The retrieved evidence discusses the general mechanisms of DNA mutations during cell division, noting that mutations can arise during both mitotic and meiotic processes, but lacks definitive comparative data across organisms to fully establish whether most mutations originate during mitosis rather than meiosis.

Evidence for · 4
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landclinic.org/-/scassets/images/org/health/articles/23095-genetic-mutations ) A genetic mutation is a change to your DNA sequence by removing, adding or replacing pieces of your DNA. What are genetic mutations? A genetic mutation is a change in a sequence of your DNA. Your DNA sequence gives your cells the information they need to perform their functions. If part of your DNA sequence is in the wrong place, isn’t complete or is damaged, you might experience symptoms of a genetic condition. Advertisement Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Policy When do genetic mutations happen? Genetic mutations occur during cell division when your cells divide and replicate. There are two types of cell division: Mitosis : The process of making new cells for your body. During mitosis, your genes instruct your cells to split into two by making a copy of your chromosomes. Meiosis : The process of making egg and sperm cells for the next generation. During meiosis, chromosomes copy themselves with half the amount of chromosomes as the original (from 46 to 23). That’s how you’re able to get your genetic material equally from each parent. How do genetic mutations happen? Genetic mutations occur during cell division. When your cells divide, they handwrite your body’s instruction manual by copying the original document word for word. There’s a lot of room for error during cell division because your cells might substitute (replace), delete (remove) or insert (add) letters while they’re copying. If you have an error (genetic mutation), your genetic instruction manual for your cells may not be readable by the cells, or may have missing parts or unnecessary parts added. All of this can mean that your cells can’t function as they normally should. Care at Cleveland Clinic Schedule Genetic Counseling Find a Doctor and Specialists Make an Appointment Function How do
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The analysis

rails:sufficiency:partial_only:for=0+4p:against=0+0p | v55:multi_partial_one_side:lean=lean_partial:for:one_sided

More for · 3
2021 · cited by 0
In contrast to common meiotic gene conversion, mitotic gene conversion, because it is so rare, is often ignored as a process influencing allelic diversity. We show that if there is a large enough number of premeiotic cell divisions, as seen in many organisms without early germline sequestration, such as plants, this is an unsafe position. From examination of 1.1 million rice plants, we determined that the rate of mitotic gene conversion events, per mitosis, is 2 orders of magnitude lower than the meiotic rate. However, owing to the large number of mitoses between zygote and gamete and because
2019 · cited by 0
Most mutations in coding regions of the genome are deleterious, causing selection to favor mechanisms that minimize the mutational load over time [1–5]. DNA replication during cell division is a major source of new mutations. It is therefore important to limit the number of cell divisions between generations, particularly for large and long-lived organisms [6–9]. The germline cells of animals and the slowly dividing cells in plant meristems are adaptations to control the number of mutations that accumulate over generations [9–11]. Fungi lack a separated germline while harboring species with ve
cited by 0
Interpreting the Dependence of Mutation Rates on Age and Time | PLOS Biology ## Figures ## Abstract Mutations can originate from the chance misincorporation of nucleotides during DNA replication or from DNA lesions that arise between replication cycles and are not repaired correctly. We introduce a model that relates the source of mutations to their accumulation with cell divisions, providing a framework for understanding how mutation rates depend on sex, age, and cell division rate. We show that the accrual of mutations should track cell divisions not only when mutations are replicative in origin but also when they are non-replicative and repaired efficiently. One implication is that observations from diverse fields that to date have been interpreted as pointing to a replicative origin of most mutations could instead reflect the accumulation of mutations arising from endogenous reactions or exogenous mutagens. We further find that only mutations that arise from inefficiently repaired lesions will accrue according to absolute time; thus, unless life history traits co-vary, the phylogenetic “molecular clock” should not be expected to run steadily across species. ## Author Summar
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held for human review11 Aug 2026
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