{"doi":"10.1093/genetics/iyac155","title":"Driving lessons: a brief (personal) history of centromere drive","abstract":"“Individuals are not stable things, they are fleeting. Chromosomes too are shuffled into oblivion, like hands of cards soon after they are dealt. But the cards themselves survive the shuffling. The cards are the genes. The genes are not destroyed by crossing-over, they merely change partners and march on. Of course they march on. That is their business.” –Richard Dawkins, The Selfish Gene (Dawkins 1976) Meiosis is an important specialized cell division in many eukaryotic species, including fungi, plants, and animals. Meiosis results in the production of haploid gametes starting from a diploid cell via 1 round of replication and 2 rounds of cell division. In an influential article published in 1957, Sandler and Novitski first pointed out that meiosis is also an intense battleground, in which gametes vie for evolutionary supremacy with each other, often poisoning their competition to gain a fratricidal advantage (Sandler and Novitski 1957). This competition, which they termed “meiotic drive,” operates as an evolutionary force that can cause an increase in frequency of the allele that is favored during meiotic transmission. Unlike alleles that rise in frequency because they confer a fitness advantage to their carriers, meiotic drivers can rise in frequency even while conferring significant fitness disadvantages on their carriers. Thus, meiotic drivers can be viewed as the quintessential selfish genes; it is the best interest of the rest of the genome to counteract their action to restore organismal fitness. With their proposal and subsequent work, Sandler and Novitski laid the foundations of the meiotic drive field. Thus, it is a special honor for me to receive the 2022 Novitski Prize for postulating that essential components of the cell division apparatus have been shaped by relentless evolutionary battles during meiosis. This essay is not intended to be a comprehensive summary of meiotic drive mechanisms but rather a personal summary of both the preceding discoveries that inspired our hypothesis and the subsequent studies that have validated and extended its key postulates. I have tried to be as historically accurate as possible while relying on an unreliable memory. In their simplest forms, meiotic drivers can be classified into 2 types (Sandler and Novitski 1957; Burt and Trivers 2006; McLaughlin and Malik 2017). The first of these acts during or after male meiosis, which normally produces 4 haploid gametes (e.g. pollen in plants, spores in fungi, sperm in animals). Meiotic drive alleles typically act by encoding toxins that prevent the survival or maturation of chromosomes that do not carry them. They protect themselves either by encoding antidotes that prevent their own destruction or by specifically targeting chromosomal “susceptibility” loci that are only carried by competing chromosomes (McLaughlin and Malik 2017). Many independent meiotic drive genes with distinct mechanisms of toxicity have been discovered in fungi, flies, plants, and mice (Olds-Clarke and Johnson 1993; Larracuente and Presgraves 2012; Lindholm et al. 2016; Saupe and Johannesson 2022). In some cases, meiotic drivers arise as neomorphic alleles that target chromosome condensation or sperm flagella functions (Merrill et al. 1999; Herrmann et al. 1999). However, the evolutionary origins of most meiotic drive genes or their toxicity mechanisms are not well understood. The second form of meiotic drive occurs in female meiosis. Unlike male meiosis, female meiosis in plants and animals is asymmetric, i.e. it produces only 1 haploid gamete per meiosis that is passed onto future generations, whereas the other 3 gametes are “evolutionary dead ends” (e.g. polar bodies in animals). This introduces a different type of competition during female meiosis. In contrast to the rampant fratricide mediated by male meiotic drivers, female meiotic drivers simply must ensure a higher-than-random probability of inclusion in the next generation. Thus, female meiotic drive incur","journal":"Genetics","year":2022,"id":294066,"datarank":0.10397207708399181,"base_score":0.6931471805599453,"endowment":0.6931471805599453,"self_citation_contribution":0.10397207708399181,"citation_network_contribution":0.0,"self_endowment_contribution":0.10397207708399181,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9492,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2022-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":341208,"name":"Harmit S. Malik","orcid":"0000-0001-6005-0016","position":0,"is_corresponding":true}],"reference_count":57,"raw_metadata":{"citation_network_status":"fetched"},"created_at":"2026-07-19T00:30:57.469517Z","pmid":"39255401","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}