Dev Bio SuperGroup Meeting

The Caenorhabditis elegans ALA neuron:its transcriptome and role in inducing sleep
Elly Chow - Sternberg Lab
Sleep is an evolutionarily conserved physiological state whose underlying mechanism
remains elusive. Caenorhabditis elegans exhibits a sleep-like state characterized by
sensory depression and locomotor quiescence in response to stress, satiety and its molting
cycle. Stress-induced sleep acts via epidermal growth factor (EGF) and EGF receptor
(EGFR) signaling, and is mediated by a single head neuron, the ALA neuron, which
expresses the EGFR ortholog LET-23. ALA differentiation is dependent on combinatorial
inputs of one LIM homeodomain transcription factor, CEH-14 (orthologous to LHX-3), and
two paired-like homeodomain transcription factors, CEH-10 and CEH-17 (both orthologous
to PRRX-2). Previous work demonstrated that ceh-14 mutants lack LET-23/EGFR and are
completely resistant to stress-induced sleep. We hypothesized that neuropeptide-encoding
genes are the downstream targets of CEH-10, CEH-14, and CEH-17 during ALA
differentiation, and that their neuropeptide products mediate stress-induced sleep. Through
characterization of the ALA transcriptome from wild-type animals and ceh-14 mutants, we
detected 8,133 protein-coding genes in the wild-type ALA, of which 382 genes were ALAenriched
and CEH-14 dependent, including 10 genes encoding neuropeptides. Using
genetic screening and conditional activation of neuropeptide genes, we identified two
FMRFamide (Phe-Met-Arg-Phe-NH2)-like neuropeptide-coding genes and one
neuropeptide-like protein-coding gene that are necessary for stress-induced sleep, and are
sufficient to induce sleep in a manner dependent on two G-coupled protein receptors
(GPCRs). In addition, a vertebrate equivalent of the FMRFamide peptides is sufficient to
induce sleep in zebrafish (Danio rerio) and C. elegans. Our results suggest that
FMRFamide peptides regulate sleep/wake behaviors throughout metazoans.

Mechanical stress and auxin transport in plant shoot apex

An Yan - Meyerowitz lab

This research explores the mechanical force control of plant morphogenesis by testing the
new theory that mechanical stress can be guiding factor for chemical signal, such as auxin.
The mechanical stress is proposed to directly regulate the localization of auxin transporter,
PIN1, thus determine the future auxin maximum site and following primordium outgrowth in
shoot apical meristem. Several sets of independent mechanical experiments support that
polarized PIN1 protein in shoot apex indeed can respond to local, non-invasive mechanical
stress changes and the cellulose/pectin cell wall is required for the PIN1 sensing of the
mechanical stress. An ethyl methanesulfonate (EMS) mutagenesis screen for phyllotactic
pattern mutant(s) is proposed to search for the sensor(s) for the PIN1 mechanical stress
sensing pathway.