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. 2021 Jan 5;217(2):iyaa037. doi: 10.1093/genetics/iyaa037

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© The Author(s) 2021. Published by Oxford University Press on behalf of Genetics Society of America.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Survival of homologous recombination InR alleles. Females. Plots represent independent trials except for repeated controls shown in (B and E), and in (C, F, and G). In all trials, wild-type and null allele controls were homologous recombinant InR^+(HR) and InR^null(HR) respectively. (A) Wild-type heterozygotes made with three accessions of ectodomain mutant InR^E19(HR). (B) Wild-type heterozygotes made with mutants of the kinase domain A-loop (InR^74(HR)) and C-terminal lobe (InR^211(HR)). (C) Wild-type heterozygotes made with mutants of kinase domain N-terminal lobe (InR^246(HR)), A-loop, KID (InR^353(HR)), and C-terminal lobe; hemizygotes shown for contrast. (D) Wild-type heterozygotes made with three accessions of the kinase insert domain mutant InR^353(HR). (E) Transheterozygotes of InR^E19(HR), InR^74(HR), and InR^211(HR). (F) Independent, replicate trails of transheterozygotes of InR^E19(HR), InR^74(HR), and InR^211(HR). (G) Transheterozygotes of InR^E19(HR), InR^74(HR), InR^246(HR) and InR^353(HR). (H) Independent, replicate trail of transheterozygotes of InR^E19(HR), InR^74(HR), InR^246(HR), and InR^353(HR). Life table summaries and proportional hazard statistics in Supplementary Table S4.