Dynamic Patterning of Maternal mRNAs in the

Asymmetric segregation of maternally-encoded proteins is essential to cell fate determination during early cell divisions of the Caenorhabditis elegans (C. elegans) embryo, but little is known about the patterning of maternal transcripts inside somatic lineages. In the first Chapter of this thesis, by detecting individual mRNA molecules in situ, we measured the densities of the two maternal mRNAs pie-1 and nos-2 in non-germline cells. We find that nos-2 mRNA degrades at a constant rate in all somatic lineages, starting approximately 1 cell-cycle after each lineage separated from the germline, consistent with a model in which the germline protects maternal mRNAs from degradation. In contrast, the degradation of pie-1 mRNAs in one somatic lineage, AB, takes place at a rate slower than that of the other lineages, leading to an accumulation of that transcript. We further show that the 3' untranslated (UTR) region of the pie-1 transcript at least partly encodes the AB-specific degradation delay. Our results indicate that embryos actively control maternal mRNA distributions in somatic lineages via regulated degradation, providing another potential mechanism for lineage specification. The evolutionary fate of an allele ordinarily depends on its contribution to host fitness. Occasionally, however, genetic elements arise that are able to gain a transmission advantage while simultaneously imposing a fitness cost on their hosts. Seidel et al. previously discovered one such element in C. elegans that gains a transmission advantage through a combination of paternal-effect killing and zygotic self-rescue. In the second Chapter of this thesis we demonstrate that this element is composed of a sperm-delivered toxin, peel-1, and an embryo-expressed antidote, zeel-1. peel-1 and zeel-1 are located adjacent to one another in the genome and co-occur in an insertion/deletion polymorphism. peel-1 encodes a novel four-pass transmembrane protein that is expressed in sperm and delivered to the embryo via specialized, sperm-specific vesicles. In the absence of zeel-1, sperm-delivered PEEL-1 causes lethal defects in muscle and epidermal tissue at the two-fold stage of embryogenesis. zeel-1 is expressed transiently in the embryo and encodes a novel six-pass transmembrane domain fused to a domain with sequence similarity to zyg-11, a substrate-recognition subunit of an