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A current perspective on the role of AGCVIII kinases in PIN-mediated apical hook development.

Willige BC, Chory J - Front Plant Sci (2015)

Bottom Line: As predicted by the Cholodny-Went theory, the cause for differential growth is the unequal distribution of the phytohormone auxin.Their localization and activity are regulated by two subfamilies of AGCVIII protein kinases: the D6 PROTEIN KINASEs as well as PINOID and its two closely related WAG kinases.This mini-review focuses on the regulatory mechanism of these AGCVIII kinases as well as their role in apical hook development of Arabidopsis thaliana.

View Article: PubMed Central - PubMed

Affiliation: Salk Institute for Biological Studies , La Jolla, CA, USA.

ABSTRACT
Despite their sessile lifestyle, seed plants are able to utilize differential growth rates to move their organs in response to their environment. Asymmetrical growth is the cause for the formation and maintenance of the apical hook-a structure of dicotyledonous plants shaped by the bended hypocotyl that eases the penetration through the covering soil. As predicted by the Cholodny-Went theory, the cause for differential growth is the unequal distribution of the phytohormone auxin. The PIN-FORMED proteins transport auxin from cell-to-cell and control the distribution of auxin in the plant. Their localization and activity are regulated by two subfamilies of AGCVIII protein kinases: the D6 PROTEIN KINASEs as well as PINOID and its two closely related WAG kinases. This mini-review focuses on the regulatory mechanism of these AGCVIII kinases as well as their role in apical hook development of Arabidopsis thaliana.

No MeSH data available.


Related in: MedlinePlus

Models describing the effects of AGCVIII kinase activity on PIN-dependent auxin efflux. Black arrows represent the direction of auxin streams. (A) and (B) Older model of PID function. (A) In cells with low PID activity (e.g., in pid loss-of-function mutants) or in cells expressing PINs with Ser to Ala mutations in the TPRXS(N/S) motifs, PINs are basally localized and therefore facilitate the downward transport of auxin. (B) In cells with high PID activity (e.g., in PID overexpressors) or in cells expressing PINs mimicking phosphorylation of the TPRXS(N/S) motifs, PIN polarity and hence the direction of auxin transport is changed. (C) to (E) Newer models of PID and D6PK functions. (C) Unphosphorylated PINs are inactive and do not facilitate auxin efflux. (D) PID kinase activity modifies PIN localization as well as PIN activity. (E) PIN phosphorylation by D6PK activates PINs without regulating PIN polarity.
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Figure 1: Models describing the effects of AGCVIII kinase activity on PIN-dependent auxin efflux. Black arrows represent the direction of auxin streams. (A) and (B) Older model of PID function. (A) In cells with low PID activity (e.g., in pid loss-of-function mutants) or in cells expressing PINs with Ser to Ala mutations in the TPRXS(N/S) motifs, PINs are basally localized and therefore facilitate the downward transport of auxin. (B) In cells with high PID activity (e.g., in PID overexpressors) or in cells expressing PINs mimicking phosphorylation of the TPRXS(N/S) motifs, PIN polarity and hence the direction of auxin transport is changed. (C) to (E) Newer models of PID and D6PK functions. (C) Unphosphorylated PINs are inactive and do not facilitate auxin efflux. (D) PID kinase activity modifies PIN localization as well as PIN activity. (E) PIN phosphorylation by D6PK activates PINs without regulating PIN polarity.

Mentions: PID overexpressors and mutants argue for a model that describes PID as a regulator of PIN localization (Figures 1A,B): Root cells that show a basal localization of PINs in the wild-type possess an accumulation of apically localized PINs in PID overexpressors. Furthermore, the apically located PIN1 protein of the shoot apex is basally localized in pid mutants (Friml et al., 2004).


A current perspective on the role of AGCVIII kinases in PIN-mediated apical hook development.

Willige BC, Chory J - Front Plant Sci (2015)

Models describing the effects of AGCVIII kinase activity on PIN-dependent auxin efflux. Black arrows represent the direction of auxin streams. (A) and (B) Older model of PID function. (A) In cells with low PID activity (e.g., in pid loss-of-function mutants) or in cells expressing PINs with Ser to Ala mutations in the TPRXS(N/S) motifs, PINs are basally localized and therefore facilitate the downward transport of auxin. (B) In cells with high PID activity (e.g., in PID overexpressors) or in cells expressing PINs mimicking phosphorylation of the TPRXS(N/S) motifs, PIN polarity and hence the direction of auxin transport is changed. (C) to (E) Newer models of PID and D6PK functions. (C) Unphosphorylated PINs are inactive and do not facilitate auxin efflux. (D) PID kinase activity modifies PIN localization as well as PIN activity. (E) PIN phosphorylation by D6PK activates PINs without regulating PIN polarity.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4593951&req=5

Figure 1: Models describing the effects of AGCVIII kinase activity on PIN-dependent auxin efflux. Black arrows represent the direction of auxin streams. (A) and (B) Older model of PID function. (A) In cells with low PID activity (e.g., in pid loss-of-function mutants) or in cells expressing PINs with Ser to Ala mutations in the TPRXS(N/S) motifs, PINs are basally localized and therefore facilitate the downward transport of auxin. (B) In cells with high PID activity (e.g., in PID overexpressors) or in cells expressing PINs mimicking phosphorylation of the TPRXS(N/S) motifs, PIN polarity and hence the direction of auxin transport is changed. (C) to (E) Newer models of PID and D6PK functions. (C) Unphosphorylated PINs are inactive and do not facilitate auxin efflux. (D) PID kinase activity modifies PIN localization as well as PIN activity. (E) PIN phosphorylation by D6PK activates PINs without regulating PIN polarity.
Mentions: PID overexpressors and mutants argue for a model that describes PID as a regulator of PIN localization (Figures 1A,B): Root cells that show a basal localization of PINs in the wild-type possess an accumulation of apically localized PINs in PID overexpressors. Furthermore, the apically located PIN1 protein of the shoot apex is basally localized in pid mutants (Friml et al., 2004).

Bottom Line: As predicted by the Cholodny-Went theory, the cause for differential growth is the unequal distribution of the phytohormone auxin.Their localization and activity are regulated by two subfamilies of AGCVIII protein kinases: the D6 PROTEIN KINASEs as well as PINOID and its two closely related WAG kinases.This mini-review focuses on the regulatory mechanism of these AGCVIII kinases as well as their role in apical hook development of Arabidopsis thaliana.

View Article: PubMed Central - PubMed

Affiliation: Salk Institute for Biological Studies , La Jolla, CA, USA.

ABSTRACT
Despite their sessile lifestyle, seed plants are able to utilize differential growth rates to move their organs in response to their environment. Asymmetrical growth is the cause for the formation and maintenance of the apical hook-a structure of dicotyledonous plants shaped by the bended hypocotyl that eases the penetration through the covering soil. As predicted by the Cholodny-Went theory, the cause for differential growth is the unequal distribution of the phytohormone auxin. The PIN-FORMED proteins transport auxin from cell-to-cell and control the distribution of auxin in the plant. Their localization and activity are regulated by two subfamilies of AGCVIII protein kinases: the D6 PROTEIN KINASEs as well as PINOID and its two closely related WAG kinases. This mini-review focuses on the regulatory mechanism of these AGCVIII kinases as well as their role in apical hook development of Arabidopsis thaliana.

No MeSH data available.


Related in: MedlinePlus