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.