Analyzing the readout of Notch signaling with single RNA precision reveals that active transcription sites are the most accurate measure of Notch-dependent transcriptional activation.

By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.

Somatic gonad architecture is regulated by innexin function, but sheath cell position does not determine germ cell exit from the stem cell pool.

Increased Notch signaling enhances germ cell reprograming in C. elegans by antagonizing PRC2-mediated repression, which results in the activation of UTX-1 and other reprograming-promoting genes.

Complementary effects of FBF-1 and FBF-2 on germline stem cell dynamics result from their distinct cooperation with mRNA deadenylase resulting in the opposite effects on the shared target mRNAs.

C. elegans germline stem cells become quiescent under starved conditions, and this quiescence maintains the stem cell state even in the absence of GLP-1/Notch signaling, which is otherwise essential for stem cell maintenance.

A previously undetected dynamic cell structure orients the mitotic spindle of germ stem cells and grows over one daughter cell, thus helping to balance niche retention with niche exit.

A Caenorhabitis elegans RNA-binding protein, FBF-2, modulates RNA sequence motif recognition through conformational change and partner protein interaction.

Nanos is required for germline specification by erasure of maternal program in primordial germ cells.

As Caenorhabditis elegans adult hermaphrodite germ cells leave the stem cell niche, they associate with a pair of somatic gonad cells that were thought to be symmetrical, but that actually take on dramatically different positions in the organ.