Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA246551 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1282200.fastq.gz | Fastqsanger.gz | |||
| SRR1282201.fastq.gz | Fastqsanger.gz |
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Project description:Stomatal abundance decrease in Arabidopsis triggered by warm-temperature is attributed to PIF4-mediated repression of SPEECHLESS (SPCH) expression. We identified the unknown developmental and transcriptional basis of this adaptive response. We analyzed stomatal lineage progression at warm- and control-T combining live-cell imaging and lineage-cell tracing with epidermal phenotyping, genetics and transcriptomics. Warm-T or PIF4 overexpression caused a fraction of stomatal precursors to lose their identity and become diverted, explaining stomatal index reduction, and hinting at developmental mechanisms underlying lineage progression. Triggering diverted precursor fate required extended exposure to warm-T, below which the process is reversible and stomatal index remains unchanged. Despite heat-induced gene reprogramming silenced key positive drivers of stomatal development as SPCH and MUTE, most lineages progressed and formed stomata. Transcriptomics revealed that warm-T shifted lineages towards uncommitted cell stages, which regained committed fates during recovery at control temperature. This indicates that stomatal development under changing temperatures occurs through partly rewired gene circuits involving alternative pathways.
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Project description:Plant tissue development often relies on the specification of cell type initials with stem cell-like properties. These later undergo differentiation, losing division potential and acquiring specific identities and functions. In the stomatal lineage, protodermal cells develop into guard cells (GCs) through the action of bHLH transcription factors (TFs) SPEECHLESS (SPCH), MUTE and FAMA. Existing models support that these regulators act sequentially, but recent evidence indicates that SPCH expression and function are retained in late stomatal cells. Here, we combine transcriptomic and genetic approaches to define SPCH's function during the late stomatal lineage. We show that relative levels and activities of SPCH and FAMA control GC division and expansion. Through cell type-specific TF induction and mRNA sequencing, we identify late-lineage targets of both TFs, and through genetic perturbation of these targets, we demonstrate that their precise temporal regulation is required for proper GC morphology and function. Our findings reveal a previously unrecognized role for SPCH in late stomatal development and support a revised model in which the functions of stomatal bHLHs are not strictly separated in time.
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