Basic Information
Gene Structure
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Domain
| Database | EntryID | E-Value | Start | end | InterPro ID | Description |
|---|
Regulation&Interaction
Annotation
Orthologous Group
| Orthologous ID | Species Number | All hits in PereRegDB | Hits of this species | Orthologous Detail |
|---|
Expression Profile
| DataSet | Number of Samples expressed(TPM>1) | Mean | Min | Max | Standard deviation(SD) | Coeffcient variation(CV) |
|---|
Pathway
| GO Term | Description | GO Category |
|---|---|---|
| GO:0000902 | cell morphogenesis | BP |
| GO:0000904 | cell morphogenesis involved in differentiation | BP |
| GO:0003674 | molecular_function | MF |
| GO:0005488 | binding | MF |
| GO:0005509 | calcium ion binding | MF |
| GO:0008150 | biological_process | BP |
| GO:0009653 | anatomical structure morphogenesis | BP |
| GO:0009888 | tissue development | BP |
| GO:0009987 | cellular process | BP |
| GO:0010026 | trichome differentiation | BP |
| GO:0010090 | trichome morphogenesis | BP |
| GO:0010091 | trichome branching | BP |
| GO:0016043 | cellular component organization | BP |
| GO:0030154 | cell differentiation | BP |
| GO:0032502 | developmental process | BP |
| GO:0032989 | cellular component morphogenesis | BP |
| GO:0043167 | ion binding | MF |
| GO:0043169 | cation binding | MF |
| GO:0046872 | metal ion binding | MF |
| GO:0048468 | cell development | BP |
| GO:0048856 | anatomical structure development | BP |
| GO:0048869 | cellular developmental process | BP |
| GO:0071840 | cellular component organization or biogenesis | BP |
| GO:0090558 | plant epidermis development | BP |
| GO:0090626 | plant epidermis morphogenesis | BP |
| KEGG Term | Name | Description |
|---|---|---|
| map04626 | Plant-pathogen interaction | Plants lack animal-like adaptive immunity mechanisms, and therefore have evolved a specific system with multiple layers against invading pathogens. The primary response includes the perception of pathogens by cell-surface pattern-recognition receptors (PRRs) and is referred to as PAMP-triggered immunity (PTI). Activation of FLS2 and EFR triggers MAPK signaling pathway that activates defense genes for antimictobial compounds. The increase in the cytosolic Ca2+ concentration is also a regulator for production of reactive oxygen species and localized programmed cell death/hypersensitive response. The secondary response is called effector-triggered immunity (ETI). Pathogens can acquire the ability to suppress PTI by directly injecting effector proteins into the plant cell through secretion systems. In addition, pathogens can manipulate plant hormone signaling pathways to evade host immune responses using coronatine toxin. Some plants possess specific intracellular surveillance proteins (R proteins) to monitor the presence of pathogen virulence proteins. This ETI occurs with localized programmed cell death to arrest pathogen growth, resulting in cultivar-specific disease resistance. |
| map04070 | Phosphatidylinositol signaling system | - |
| map03420 | Nucleotide excision repair | Nucleotide excision repair (NER) is a mechanism to recognize and repair bulky DNA damage caused by compounds, environmental carcinogens, and exposure to UV-light. In humans hereditary defects in the NER pathway are linked to at least three diseases: xeroderma pigmentosum (XP), Cockayne syndrome (CS), and trichothiodystrophy (TTD). The repair of damaged DNA involves at least 30 polypeptides within two different sub-pathways of NER known as transcription-coupled repair (TCR-NER) and global genome repair (GGR-NER). TCR refers to the expedited repair of lesions located in the actively transcribed strand of genes by RNA polymerase II (RNAP II). In GGR-NER the first step of damage recognition involves XPC-hHR23B complex together with XPE complex (in prokaryotes, uvrAB complex). The following steps of GGR-NER and TCR-NER are similar. |