Methamphetamine exposure induces neuronal programmed necrosis by activating the receptor‐interacting protein kinase 3 ‐related signalling pathway

Autophagy is a conserved cellular degradative process important for cellular homoeostasis and survival. An early committal step during the initiation of autophagy requires the actions of a protein kinase called ATG1 (autophagy gene 1). In mammalian cells, ATG1 is represented by ULK1 (uncoordinated-51-like kinase 1), which relies on its essential regulatory cofactors mATG13, FIP200 (focal adhesion kinase family-interacting protein 200 kDa) and ATG101. Much evidence indicates that mTORC1 [mechanistic (also known as mammalian) target of rapamycin complex 1] signals downstream to the ULK1 complex to negatively regulate autophagy. In this chapter, we discuss our understanding on how the mTORC1–ULK1 signalling axis drives the initial steps of autophagy induction. We conclude with a summary of our growing appreciation of the additional cellular pathways that interconnect with the core mTORC1–ULK1 signalling module.

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Faculty Opinions recommendation of A protein kinase target of a PDK1 signalling pathway is involved in root hair growth in Arabidopsis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1020408.234459 ◽

2004 ◽

Author(s):

Jen Sheen

Keyword(s):

Protein Kinase ◽

Root Hair ◽

Hair Growth ◽

Signalling Pathway ◽

Root Hair Growth

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Faculty Opinions recommendation of A collective form of cell death requires homeodomain interacting protein kinase.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1090216.543437 ◽

2007 ◽

Author(s):

Kristin White

Keyword(s):

Cell Death ◽

Protein Kinase ◽

Interacting Protein

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Activation of the protein kinase B and glycogen synthase kinase-3 signalling pathway during transient differentiation of human colon cancer HT-29 cells

Collection Symposium Series ◽

10.1135/css199903019 ◽

1999 ◽

Author(s):

Zdena Tuháčková ◽

Eva Šloncová ◽

Jan Hlaváček ◽

Vlasta Sovová ◽

Jiří Velek

Keyword(s):

Colon Cancer ◽

Protein Kinase ◽

Glycogen Synthase ◽

Protein Kinase B ◽

Human Colon ◽

Signalling Pathway ◽

Glycogen Synthase Kinase ◽

Glycogen Synthase Kinase 3 ◽

Human Colon Cancer ◽

Ht 29

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Pseudomonas syringae Effector AvrPphB Suppresses AvrB-Induced Activation of RPM1 but Not AvrRpm1-Induced Activation

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-08-14-0248-r ◽

2015 ◽

Vol 28 (6) ◽

pp. 727-735 ◽

Cited By ~ 24

Author(s):

Andrew R. Russell ◽

Tom Ashfield ◽

Roger W. Innes

Keyword(s):

Disease Resistance ◽

Protein Kinase ◽

Molecular Mechanism ◽

Pseudomonas Syringae ◽

Hypersensitive Response ◽

Hypersensitive Resistance ◽

Nicotiana Glutinosa ◽

Resistance Response ◽

Interacting Protein ◽

Soybean Plants

The Pseudomonas syringae effector AvrB triggers a hypersensitive resistance response in Arabidopsis and soybean plants expressing the disease resistance (R) proteins RPM1 and Rpg1b, respectively. In Arabidopsis, AvrB induces RPM1-interacting protein kinase (RIPK) to phosphorylate a disease regulator known as RIN4, which subsequently activates RPM1-mediated defenses. Here, we show that AvrPphB can suppress activation of RPM1 by AvrB and this suppression is correlated with the cleavage of RIPK by AvrPphB. Significantly, AvrPphB does not suppress activation of RPM1 by AvrRpm1, suggesting that RIPK is not required for AvrRpm1-induced modification of RIN4. This observation indicates that AvrB and AvrRpm1 recognition is mediated by different mechanisms in Arabidopsis, despite their recognition being determined by a single R protein. Moreover, AvrB recognition but not AvrRpm1 recognition is suppressed by AvrPphB in soybean, suggesting that AvrB recognition requires a similar molecular mechanism in soybean and Arabidopsis. In support of this, we found that phosphodeficient mutations in the soybean GmRIN4a and GmRIN4b proteins are sufficient to block Rpg1b-mediated hypersensitive response in transient assays in Nicotiana glutinosa. Taken together, our results indicate that AvrB and AvrPphB target a conserved defense signaling pathway in Arabidopsis and soybean that includes RIPK and RIN4.

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The CBL-Interacting Protein Kinase NtCIPK23 Positively Regulates Seed Germination and Early Seedling Development in Tobacco (Nicotiana tabacum L.)

Plants ◽

10.3390/plants10020323 ◽

2021 ◽

Vol 10 (2) ◽

pp. 323

Author(s):

Sujuan Shi ◽

Lulu An ◽

Jingjing Mao ◽

Oluwaseun Olayemi Aluko ◽

Zia Ullah ◽

...

Keyword(s):

Protein Kinase ◽

Seed Germination ◽

Seedling Growth ◽

Hypocotyl Elongation ◽

Interacting Protein ◽

Knock Out ◽

Early Seedling Growth ◽

Tobacco Seedlings ◽

Early Seedling ◽

Cotyledon Expansion

CBL-interacting protein kinase (CIPK) family is a unique group of serine/threonine protein kinase family identified in plants. Among this family, AtCIPK23 and its homologs in some plants are taken as a notable group for their importance in ions transport and stress responses. However, there are limited reports on their roles in seedling growth and development, especially in Solanaceae plants. In this study, NtCIPK23, a homolog of AtCIPK23 was cloned from Nicotiana tabacum. Expression analysis showed that NtCIPK23 is mainly expressed in the radicle, hypocotyl, and cotyledons of young tobacco seedlings. The transcriptional level of NtCIPK23 changes rapidly and spatiotemporally during seed germination and early seedling growth. To study the biological function of NtCIPK23 at these stages, the overexpressing and CRISPR/Cas9-mediated knock-out (ntcipk23) tobacco lines were generated. Phenotype analysis indicated that knock-out of NtCIPK23 significantly delays seed germination and the appearance of green cotyledon of young tobacco seedling. Overexpression of NtCIPK23 promotes cotyledon expansion and hypocotyl elongation of young tobacco seedlings. The expression of NtCIPK23 in hypocotyl is strongly upregulated by darkness and inhibited under light, suggesting that a regulatory mechanism of light might underlie. Consistently, a more obvious difference in hypocotyl length among different tobacco materials was observed in the dark, compared to that under the light, indicating that the upregulation of NtCIPK23 contributes greatly to the hypocotyl elongation. Taken together, NtCIPK23 not only enhances tobacco seed germination, but also accelerate early seedling growth by promoting cotyledon greening rate, cotyledon expansion and hypocotyl elongation of young tobacco seedlings.

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