Biology subjects

Smit, M. E.

Publications and source records attributed to Smit, M. E..

4 recordsLinked to original sources

bioRxiv2026

ERECTA signaling controls the timing of Arabidopsis Guard Cell maturation at the embryonic leaf tip

While cell identities are established early during embryogenesis, these cells remain immature until germination, and the mechanisms enforcing this developmental pause are poorly understood. Embryonic stomatal cells provide a model to study this pause as the stomatal transcription factor FAMA, normally sufficient for Guard Cell maturation in seedlings, can not drive maturation in the Arabidopsis embryo. Here we show that FAMAs ability to drive maturation depends on leaf polarity and adaxial stomatal cells can progress further in their lineage. We next find that ERECTA-family receptor signaling, which controls stomatal patterning, also suppresses embryonic stomatal maturation. In er erl1 erl2 mutants, cell pairs at the cotyledon tip acquire characteristics of maturing guard cells: cell wall reinforcement, pore-associated thickening, and expression of late lineage markers as identified by whole embryo transcriptomics. This precocious maturation however remains incomplete: many GC markers remain absent, and cells lack an open pore and mature vacuoles. Genetic analysis shows that partial maturation requires but is not limited by low levels of FAMA. Restriction of maturation to the cotyledon tip correlates with locally elevated ERECTA-family receptor abundance, while high auxin appears dispensable for this. Finally, we show that EPFL-ER signaling mediates leaf tip Guard Cell size postembryonically as well. Altogether, we identify ERECTA signaling as a local brake on embryonic stomatal cell maturation, discovering another way to push precocious stomatal cell maturation that results in a complex, partially mature cell state that provide insights into the limitations on cell embryonic cell maturation.

plant biology↗

bioRxiv2025

Transcriptional targets of SPEECHLESS and FAMA control guard cell division and expansion in the late stomatal lineage

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 SPCHs 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.

plant biology↗

bioRxiv2022

De novo stem cell establishment in meristems requires repression of organ boundary cell fate

Stem cells play important roles in animal and plant biology as they sustain morphogenesis and tissue replenishment following aging or injuries. In plants, stem cells are embedded in multicellular structures called meristems and the formation of new meristems is essential for the plastic expansion of the highly branched shoot and root systems. In particular, axillary meristems that produce lateral shoots arise from the division of boundary domain cells at the leaf base. The CUP-SHAPED COTYLEDON (CUC) genes are major determinants of the boundary domain and are required for axillary meristem initiation. However, how axillary meristems get structured and how stem cells become established de novo remains elusive. Here, we show that two NGATHA-LIKE transcription factors, DPA4 and SOD7, redundantly repress CUC expression in the initiating axillary meristem. Ectopic boundary fate leads to abnormal growth and organisation of the axillary meristem and prevents de novo stem cell establishment. Floral meristems of the dpa4 sod7 double mutant show a similar delay in stem cell de novo establishment. Altogether, while boundary fate is required for the initiation of axillary meristems, our work reveals how it is later repressed to allow proper meristem establishment and de novo stem cell niche formation.

plant biology↗

bioRxiv2018

A network of transcriptional repressors mediates auxin response specificity

INTRODUCTORY PARAGRAPHThe regulation of signalling capacity plays a pivotal role in setting developmental patterns in both plants and animals (1). The hormone auxin is a key signal for plant growth and development that acts through the AUXIN RESPONSE FACTOR (ARF) transcription factors (2). A subset of these ARFs comprises transcriptional activators of target genes in response to auxin, and are essential for regulating auxin signalling throughout the plant lifecycle (3). While ARF activators show tissue-specific expression patterns, it is unknown how their expression patterns are established. Chromatin modifications and accessibility studies revealed the chromatin of loci encoding ARF activators is constitutively open for transcription. Using a high-throughput yeast one-hybrid (Y1H) approach, we discovered a network of transcriptional regulators of ARF activator genes from Arabidopsis thaliana. Expression analyses demonstrated that the majority of these regulators act as repressors of ARF transcription in planta. Our observations support a scenario where the default configuration of open chromatin enables a network of transcriptional repressors to shape the expression pattern of ARF activators and provide specificity in auxin signalling output throughout development.

plant biology↗