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S1E8 | Joseph Cammarata | Cytokinin-CLAVATA cross-talk regulates shoot meristem

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Manage episode 326404940 series 3299153
Content provided by Arif Ashraf. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by Arif Ashraf or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://player.fm/legal.

Article: Cytokinin–CLAVATA cross-talk is an ancient mechanism regulating shoot meristem homeostasis in land plants
Journal: PNAS
Year: 2022
Guest: Joseph Cammarata
Host: Arif Ashraf

Abstract

Plant shoots grow from stem cells within shoot apical meristems (SAMs), which produce lateral organs while maintaining the stem cell pool. In the model flowering plant Arabidopsis, the CLAVATA (CLV) pathway functions antagonistically with cytokinin signaling to control the size of the multicellular SAM via negative regulation of the stem cell organizer WUSCHEL (WUS). Although comprising just a single cell, the SAM of the model moss Physcomitrium patens (formerly Physcomitrella patens) performs equivalent functions during stem cell maintenance and organogenesis, despite the absence of WUS-mediated stem cell organization. Our previous work showed that the stem cell–delimiting function of the receptors CLAVATA1 (CLV1) and RECEPTOR-LIKE PROTEIN KINASE2 (RPK2) is conserved in the moss P. patens. Here, we use P. patens to assess whether CLV–cytokinin cross-talk is also an evolutionarily conserved feature of stem cell regulation. Application of cytokinin produces ectopic stem cell phenotypes similar to Ppclv1a, Ppclv1b, and Pprpk2 mutants. Surprisingly, cytokinin receptor mutants also form ectopic stem cells in the absence of cytokinin signaling. Through modeling, we identified regulatory network architectures that recapitulated the stem cell phenotypes of Ppclv1a, Ppclv1b, and Pprpk2 mutants, cytokinin application, cytokinin receptor mutations, and higher-order combinations of these perturbations. These models predict that PpCLV1 and PpRPK2 act through separate pathways wherein PpCLV1 represses cytokinin-mediated stem cell initiation, and PpRPK2 inhibits this process via a separate, cytokinin-independent pathway. Our analysis suggests that cross-talk between CLV1 and cytokinin signaling is an evolutionarily conserved feature of SAM homeostasis that preceded the role of WUS in stem cell organization.

Cover art design and audio editing: Ragib Anjum

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27 episodes

Artwork
iconShare
 
Manage episode 326404940 series 3299153
Content provided by Arif Ashraf. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by Arif Ashraf or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://player.fm/legal.

Article: Cytokinin–CLAVATA cross-talk is an ancient mechanism regulating shoot meristem homeostasis in land plants
Journal: PNAS
Year: 2022
Guest: Joseph Cammarata
Host: Arif Ashraf

Abstract

Plant shoots grow from stem cells within shoot apical meristems (SAMs), which produce lateral organs while maintaining the stem cell pool. In the model flowering plant Arabidopsis, the CLAVATA (CLV) pathway functions antagonistically with cytokinin signaling to control the size of the multicellular SAM via negative regulation of the stem cell organizer WUSCHEL (WUS). Although comprising just a single cell, the SAM of the model moss Physcomitrium patens (formerly Physcomitrella patens) performs equivalent functions during stem cell maintenance and organogenesis, despite the absence of WUS-mediated stem cell organization. Our previous work showed that the stem cell–delimiting function of the receptors CLAVATA1 (CLV1) and RECEPTOR-LIKE PROTEIN KINASE2 (RPK2) is conserved in the moss P. patens. Here, we use P. patens to assess whether CLV–cytokinin cross-talk is also an evolutionarily conserved feature of stem cell regulation. Application of cytokinin produces ectopic stem cell phenotypes similar to Ppclv1a, Ppclv1b, and Pprpk2 mutants. Surprisingly, cytokinin receptor mutants also form ectopic stem cells in the absence of cytokinin signaling. Through modeling, we identified regulatory network architectures that recapitulated the stem cell phenotypes of Ppclv1a, Ppclv1b, and Pprpk2 mutants, cytokinin application, cytokinin receptor mutations, and higher-order combinations of these perturbations. These models predict that PpCLV1 and PpRPK2 act through separate pathways wherein PpCLV1 represses cytokinin-mediated stem cell initiation, and PpRPK2 inhibits this process via a separate, cytokinin-independent pathway. Our analysis suggests that cross-talk between CLV1 and cytokinin signaling is an evolutionarily conserved feature of SAM homeostasis that preceded the role of WUS in stem cell organization.

Cover art design and audio editing: Ragib Anjum

  continue reading

27 episodes

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