Open AccessUncoupling Different Characteristics of the C. elegans E Lineage from Differentiation of Intestinal Markers
Author(s) -
Scott Robertson,
Jessica Medina,
Rueyling Lin
Publication year - 2014
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0106309
Subject(s) - biology , microbiology and biotechnology , cellular differentiation , cell division , cell fate determination , genetics , embryo , lineage (genetic) , transcription factor , cell , gene
In the 4-cell C. elegans embryo, a signal from P 2 to its anterior sister, EMS, specifies the posterior daughter of EMS, E, as the sole founder cell for intestine. The P 2 -to-EMS signal restricts high level zygotic expression of the redundant GATA transcription factors, END-1 and END-3, to only the E lineage. Expression of END-1 or END-3 in early blastomeres is sufficient to drive intestinal differentiation. We show here that a number of E lineage characteristics, which are also regulated through P 2 -EMS signaling, can be uncoupled from intestine development, and each with a different sensitivity to specific perturbations of the P 2 -EMS signal. For example, we show that the extended cell cycle in Ea and Ep depends on the P 2 -induced high level expression of the cell cycle regulator, WEE-1.1, in E. A mutation in wee-1.1 results in shortened Ea and Ep cell cycles, but has no effect upon intestinal differentiation or embryogenesis. Furthermore, it has been shown previously that the total number of E lineage cell divisions is regulated by a mechanism dependent upon E being specified as the intestinal founder cell. We now show, however, that cell division counting can be uncoupled from intestine differentiation in the E lineage. Many mutations in P 2 -EMS signal genes exhibit nonfully-penetrant defects in intestinal differentiation. When embryos with those mutations generate intestinal cells, they often make too many intestinal cells. In addition, at the level of individual embryos, expression of end-1 and end-3 , and another very early E-specific zygotic gene, sdz-23 , exhibit stochastic and discordant defects in P 2 -EMS signaling mutants. We show here that sdz-23 is expressed close to wildtype levels in embryos deleted of both end-1 and end-3 . sdz-23 does not appear to function in intestine development, raising the intriguing possibility that the P 2 -EMS interaction has downstream molecular consequences within the E lineage independent of end-1/3 and intestinal development.