Takashi ISHIDA

Dr. Takashi ISHIDA

Associate Professor, Faculty of Advanced Science and Technology

Research Fields
Plant stem cell and development

Research interest

I. Analyses of peptide hormone mediated intercellular communications in shoot meristem.

Coordinated cell proliferation and cell differentiation are essential processes in multicellular organisms. To achieve these functions, organisms have developed scrupulously designed cell-to-cell communication systems over the course of evolution. Plants have established unique ligand-receptor-based signaling modules, such as the CLAVATA (CLV) pathway, which comprises the CLV3 peptide hormone and the extracellular leucine-rich repeat (LRR) domain-containing receptors. In the shoot apical meristem (SAM) of Arabidopsis thaliana (Arabidopsis), CLV signal transducers and WUSCHEL (WUS), a homeobox transcription factor, form a negative feedback loop that controls the number of stem cells.
Recently, I have showed that the Arabidopsis G protein beta-subunit1 (AGB1) is involved in the CLV signaling pathway. agb1 mutant exhibits an enlarged SAM and increased number of carpel, similar to that of clv mutants. We are aiming to elucidate further molecular insights of these proteins.
Reference : Ishida et al., EMBO rep, 2014

II. Exploring molecular machineries that regulate stem cell activities in root meristem.

Coordination between cell proliferation and cell differentiation is important also in root meristem. Plants require the cell-to-cell communication system to regulate their activities and to ensure for precise postembryonic development. Shoot and root systems are thought to share common mechanism for carrying out this process; however, its molecular basis is largely unclear. It has been suggested that synthetic CLV3/ EMBRYO SURROUNDING REGION (CLE) peptide treatment shrank the root meristem through the CLV-related receptors in Arabidopsis.
I have identified several molecules that are involved in the CLV-like signaling pathway in root, e.g. BAM1, RPK2 and PUB4. Mutation in these genes decreased sensitivity to the CLE-peptides. Further, we have found that several signaling factors are expressed in limited cells of the root meristem, suggesting that these cells may be responsible for the CLE peptide-stimulated shrinkage of root meristem. We are deciphering what types of cells are involved in the regulatory mechanisms in the root meristem.
Reference : Kinoshita et al., Development, 2015; Shimizu et al., New phytol, 2015

III. Phytoparasitic nematodes hijack vascular stem cells

The developmental plasticity is one of the most striking features of plant morphogenesis, as plants are able to vary their shapes in response to environmental cues. Biotic or abiotic stimuli often promote organogenesis in plants that is not observed under normal growth conditions. Root-knot nematodes (RKNs) are known to parasitize multiple species of rooting plants and to induce characteristic tissue expansion called galls or root-knots (RKs), on the roots of their hosts by perturbing the plant cellular machinery. RKs contain giant cells (GCs) and neighboring cells (NCs), and the GCs are a source of nutrients for the parasitizing nematode. Highly activated cell proliferation was observed in galls. However, the underlying mechanisms that regulate the symptoms that are triggered by the plant-animal interaction have not yet been elucidated.
We have established in vitro infection assay system with Meloidogyne incognita. By utilizing the in vitro system, we are trying to understand how the nematodes modulate developmental regulation mechanisms of plant cells to ensure the atypical cell proliferation and GC formation during the infection processes.
Yamaguchi et al., Front Plant Sci, 2017



2021年4月9日 熊本大など 菌由来の除草剤開発化学工業日報
(Related to a publication: Ishida et al., Scientific Reports 2021)



Oct. 12, 2021 United States Patent, Patent number: US 11,142,497 B2, Plant growth suppression agent, and plant growth suppression method using same
Hayato Ishikawa, Tokio Tani, Shinichiro Sawa, Takashi Ishida, Yusuke Fukushima, Jun Inagaki



Technician Mika YOSHIMURA
Page top