During ascogenesis in Neurospora, the ascospores are partitioned at the eight-nucleus stage that follows meiosis and apost-meiotic mitosis, and the ascospores that form in eight-spored asci are usually homokaryotic. We had previouslycreated novel TNt strains by introgressing four Neurospora crassa insertional translocations (EB4, IBj5, UK14-1, andB362i) into N. tetrasperma. We now show that crosses of all the TNt strains with single-mating-type derivatives of thestandard N. tetrasperma pseudohomothallic strain 85 (viz. TNta × 85A or TNtA × 85a) can produce rare eight-sporedasci that contain heterokaryotic ascospores, or ascospores with other unexpected genotypes. Our results suggest thatthese rare asci result from the interposition of additional mitoses between the post-meiotic mitosis and the partitioningof nuclei into ascospores, leading to the formation of supernumerary nuclei that then generate the heterokaryoticascospores. The rare asci probably represent a background level of ascus dysgenesis wherein the partitioning ofascospores becomes uncoupled from the post-meiotic mitosis. Ordinarily, the severest effect of such dysgenesis, theproduction of mating-type heterokaryons, would be suppressed by the N. crassa tol (tolerant) gene, thus explainingwhy such dysgenesis remained undetected thus far.

The vertebrate inner nuclear membrane protein, lamin B receptor, has an N-terminal *200 residue nucleoplasmic domain(NTD), and a *420 residue C-terminal domain (CTD) that anchors the NTD to the INM. Chen et al (2016) showed theNTD interacts with Xist long noncoding RNA to effect X chromosome inactivation in female mammals. Tsai et al (2016)showed the CTD has sterol reductase activity that is essential for viability. And Nikolakaki et al (2017) proposed a model tointerconnect these disparate functions of this chimeric protein. It amuses me now to think back to 24 years ago, when I wasconcerned that these domains might have come together in a cloning artifact.

The ${T(EB4)}^{Nt}a$, ${T(IBj5)}^{Nt}a$, and ${T(B362i)}^{Nt}A$ strains were constructed by introgressing the insertional translocations EB4, IBj5, and B362i from Neurospora crassa into the related species N. tetrasperma. Theprogeny from crosses of ${T(IBj5)}^{Nt}a$ and ${T(B362i)}^{Nt}A$ with opposite mating-type derivatives of the standard N. tetrasperma strain 85 exhibited a unique and unprecedented transmission ratio distortion (TRD) that disfavored homokaryons produced following alternate segregation relative to those produced following adjacent-1 segregation. The TRD was not evident among the [mat A + mat a] dikaryons produced following either segregation. Further, crosses of the ${T(IBj5)}^{Nt}a$ and ${T(B362i)}^{Nt}A$ strains with the Eight spore (E) mutant showed an unusual ascus phenotype called ‘max-4’. We propose that the TRD and the max-4 phenotype are manifestations of the same Bateson-Dobzhansky-Muller incompatibility (BDMI). Since the TRD selects against 2/3 ofthe homokaryotic progeny from each introgression cross, the BDMI would have enriched for the dikaryotic progeny in the viable ascospores, and thus, paradoxically, facilitated the introgressions.

Segregation distortion refers to an unusual genetic phenomenon in diploid organisms by which the two alleles at a locus in a parent are not recovered in the classical 1:1 Mendelian ratio in its offspring. The Drosophila melanogaster neogene Sd was created by a duplication breakpoint on the left arm of chromosome 2 (2L), and encodes a truncated RanGAP protein with normal GTPase activity but which mis-localizes to the nucleus and disrupts Ran gradients. Male flies carrying Sd exhibit segregation distortion for the Rsp locus on the right arm of chromosome 2 (2R). Specifically, spermatids inheriting chromosome 2 with the Sd⁺ Rsp^s(s) genotype, in heterozygous males of genotype Sd Rspⁱ /Sd⁺ Rsp^s(s), fail to develop properly so that the majority of progeny (approaching 100%) carry just the Sd Rspⁱ chromosome. One recent paper reported novel RNAi-expressing transgenes with Sd-mimicking properties; and another reported localization of an X-linked suppressor which restores Mendelian transmission. This article highlights how Drosophila genetics resources made this possible, and the significance of these findings to nucleus-cytoplasm transactions of interest to the wider cell biology community.