AT5G16560

Gene Details

Gene ID: AT5G16560
Gene Symbol: KAN, KAN1
Gene Name: KANADI, KANADI 1
Description: Homeodomain-like superfamily protein;(source:Araport11)
TAIR Accession:
Genome: Araport11_genome_release
Species: Arabidopsis thaliana

Functional Descriptions

PO:0000015 — cotyledon primordium — cotyledon primordia (exact, plural), portion of cotyledon primordium tissue (exact), primordio de cotiledón (Spanish, exact), 子葉原基（可視的）(Japanese, exact)
PO:0004703 — carpel primordium — carpel primordia (exact, plural), portion of carpel primordium tissue (exact), primordio de carpelo (Spanish, exact), 心皮原基(可視的） (Japanese, exact)
PO:0009009 — plant embryo — embrión (Spanish, exact), 植物胚 (Japanese, exact), germ (related), embryo (broad)
PO:0009035 — nectary — nectario (Spanish, exact), 蜜腺 (Japanese, exact)
PO:0005417 — phloem — floema (Spanish, exact), portion of phloem tissue (exact), 師部、師管 (Japanese, exact)
PO:0009005 — root — raíz (Spanish, exact), radices (exact, plural), radix (exact), 根 (Japanese, exact), aerial root (narrow), climbing root (narrow)

CS24283 — the first two leaves of mutant plants are slightly uprolled and usually produce abaxial trichomes; the polarity of the mesophyll is also affected.
CS24284 — Null allele of KANADI. Mutation consists of a 12 kb deletion that removes the KAN promoter; the first two leaves of mutant plants are slightly uprolled and usually produce abaxial trichomes; the polarity of the mesophyll is also affected.
CS67887 — Produces abaxial trichomes precociously, leaves curled upwards, or flatter than normal
CS67888 — Produces abaxial trichomes precociously; kan1 kan2 double mutants have small, up-curled leaves with abaxial protrusions, and are sterile.
bop1-4 bop2-11 kan1-2 kan2-1 — About nine-tenths of the mutants exhibited abaxialized vasculature. The exclusively adaxialized vasculature observed in kan1 kan2 petioles was not detected in bop1 bop2 kan1 kan2 petioles. The radialized portion of bop1 bop2 kan1 kan2 leaves showed various kinds of organ polarity defects. The vascular bundles of nearly half of the leaves (44.0%) consisted of phloem surrounded by xylem, while one-third (36.0%) displayed xylem surrounded by phloem, and a small percentage (16.0%) had a mixture of both types of vasculature.
bop1-4 bop2-11 kan1-2 kan2-1 — Quadruple mutant plants developed narrow leaves with ectopic blade outgrowth along the petioles, like bop1 bop2 leaves, as well as ectopic outgrowths on their abaxial lamina, like kan1 kan2 leaves. However, all of the bop1 bop2 kan1 kan2 leaves also showed extended, radialized petiole development that was not observed in either parental genotype.
bop1-4 bop2-11 kan1-2 kan2-1 — bop1 bop2 kan1 kan2 stems had a decreased ratio of adaxialized vascular phenotypes compared with kan1 kan2 stems. Similar to what was observed in petioles, 6.7% of bop1 bop2 kan1 kan2 stems exhibited an abaxialized phenotype of xylem surrounded by phloem, while others (13.3%) had both types of vasculature in a single stem.
crc-1 kan1-2 — Ectopic adaxial tissues are restricted to the medial domain of the carpels, normally occupied by the abaxial replum. Formation of external ovule-bearing placentae.
kan — Altered abaxial identity in leaves and carpels
kan1 kan2 ats — Similar to kan1 kan2 double mutant. However, the ovules have a novel phenotype, forming a single amorphous structure in place of both integuments.
kan1-2 — A few external ovules develop at the base of the gynoecium and straps of ectopic style from along the abaxial replum. Phenotype is present primarily in the first formed carpels.
kan1-2 kan2-1 — All kan1 kan2 stem vascular bundles displayed phloem surrounded by xylem, indicating adaxialized polarity.
kan1-2 kan2-1 — Cotyledons are narrow, cup-shaped and point upward. Leaves are narrow, dark green and develop ectopic outgrowths on their abaxial side only. Four to six stipules, rather than two, develop at the base of each leaf, surrounding its entire circumference. Stems fail to elongate upon flowering. Floral organ morphology is highly abnormal. Mature ovules have reduced outer integuments. Aberrant positioning of cell types, primarily along the adaxial/abaxial lateral organ axis.
kan1-2 kan2-1 — Double mutant plants have narrow leaves and developed ectopic outgrowths on their abaxial lamina.
kan1-2 kan2-1 — External structures of the carpel are largely absent. Ovules arise from a surface or column of tissue at the center of the flower. The inner integuments of these ovules are normal but the asymmetrical outer integument is now a nearly symmetrical and relatively amorphous collar of tissue.
kan1-2 kan2-1 — The vasculature in more than half (55.9%) of kan1 kan2 leaf petioles exhibited a pattern of phloem surrounded by xylem, representing an adaxialized phenotype. However, very surprisingly, 17.6% of kan1 kan2 leaf petioles had abaxialized vasculature or a mixture of adaxialized and abaxialized vasculature.
kan1-2/kan2-1/kan4-3 — Radialized leaf like organs form on the hypocotyl. Altered stomata and root hair pattering.Increased periclinal divisions on abaxial side of cotyledons and hypocotyl.Ectopic expression of PIN1 in hypocotyl region.
pgy1-1/as1-1/kan1 — Triple mutant.as1/pgy1 phenotype is supressed and leaves are more rounded and do not form ectopic lamina.
pgy1-1/kan1-2/kan2-1 — kan1/kan2 defects in gynoecium development is mostly supressed. Plants are fertile and siliques more elongated compared to the kan1/kan2 double mutant and only occasionally form ectopic style tissue along the replum.Leaves are small and adaxialized.

Functional Keywords

Literature and News

Gene Resources

Sequences

cDNA Sequence

>AT5G16560.1
TGGGTTTACTTGTTGAAAGGTGAAAAAGACAAATTGAAATACCATCCCAAAATAAAATAAAAAGCTTCCAATATTTGGAATATAGCGAATGACAATATTACCCTTTCTCAACTATCGTTTTCCAAGATATACTCTCGAGGAACAACATCTCACACATACACATACACATACATGTACATGAACGAACACACATATATCTCTCTCTCTTACCTGTTTTTAATTTTCCTGGATTTAGTTTTATTCCTTTTTTCTCTTCTGCCTTTGCTTCACAACACACATACCTCTCTCTATCTCTCTCTTCCTTCTTTTTCTCTCTCTCTGCGTCTTACTTTGAGCATGTTTGTTTCTTCAAGAAGATCATCACTCAACTTCTCTCTCTTCTTCTAAGCTTCTCTTTAACTTCATCTCTCTCACTTTCTCCTTTCTTTCTGAGATATAGAGAGAGAAAGAGAACAAAAAAAATATCAAATCTTTCAGACACCCTTTTGACTTCTTTGCCTAAAGAATCTCTCTGCTTTCTCTTCTCCTTAGAGAAAATCATTTTAAATTCCTAAGCAAAACCCTCAGGAGAAAAAAAAAACAAAAGAATAGTCATCATCATCATCACCATCATCATCCTTATCATCATCAACAACTTCAGTGGCAGCAATAGCAAGAGAAAGGTTTCTTTAATTATGTCTATGGAAGGTGTTTTTCTAGAGAAAACCAAAACAAACACAACAACTACTCTCCCTGATCTATCTCTCCACATCAGTCTCCCAGATATTCATCAATACCATCACAATGAATCTTCTAAAGAATCTTCAAGAAGATCCTCCCAACTCGAAAACAACAACCGATCGTCCAACTTTGAACTCTCTTTATCTCATCATAACCATCCAACAGCAAGAATCTTCCATTGTCCTGATCGAAGAACCCTTAATCTTCCTCATCAGCAGCATTACAACAACCCTATCATCAATGGTGTTCATCAAAGGGTCGATGAATCCGAGATTAGTAATCTCCACCGTCCAATTAGAGGCATCCCGGTCTATCACAACCGTTCATTCCCTTTCCACCAACAAAACTCTTCATTACCTTCTCTTGGAGGAGGAGACATGGATCAAATCTCAATCTTAAACTCATCTTCCGGCTACAACAACGCTTACCGATCATTACAATCTTCCCCGAGGCTTAAAGGTGTTCCTTTGCATCATCATCATCATCATAATCAGTATGGAGTCGTTGGATCTTCAGATTCGTCTTCTCCTCATCACCATAACCATCATCATCATGGGATGATCAGATCAAGATTCTTGCCTAAGATGCCGACAAAGCGAAGCATGAGAGCTCCAAGGATGCGTTGGACTAGTAGCCTCCACGCGCGGTTTGTTCACGCTGTTGAGCTTCTAGGCGGCCATGAAAGAGCAACTCCAAAGTCGGTTCTTGAGCTCATGGATGTAAAAGACTTAACTTTAGCACATGTGAAGAGCCATTTGCAGATGTATCGAACTGTTAAGACCACTAACAAGCCTGCTGCTTCATCAGATGGGTCAGGAGAAGAAGAAATGGGCATAAATGGAAACGAAGTTCATCATCAATCATCGACGGATCAAAGGGCACAATCTGATGATACTTCTCTTCATCAAGAAACTGACATTTCTTCCACACAACCTCGTTGGAGTAACTCTTCACGAGAGACATGGCCATTAAGTAATAACTGCTCAAGCGACATAGATACAATGATCAGAACTTCATCAACATCAATGATCTCTCATTATCAAAGATCCAGCATTCAAAATCAGGAGCAAAGGTCGAATGATCAAGCAAAGAGGTGTGGAAATCTTAGTTGTGAAAATCCAAGTTTGGAGTTTACATTAGGCAGACCAGATTGGCACGAGAAATGACTTTCTTGATCAATTTGGATTTTTATATATATTGGATTTTTTATTTTTTTGTTTCATCTTTCTCTCTCTATATATACTCAGAAACATGTATGCAGTATATATCTTTGTGACGATGAAATTCTCAGCGTAAAAGAAGGAGAACACGTAGAGAGCCAAGCTGCTCAAGAGTGTTGATTTTTGCACAGAGAGAGAGAATATCACTACCAAAATGAAGAAATTTGGAGGTTCCTCTTCTCAAGTTCCATTGATGATTTGATTATAAAGTGGATGATCAATGTATGAGTTTTTGTTTTTGGGTTTTCGGGTTTTTAGTTTTTTGAGGTTGATCTGGTGGTGTGATCATAAGTTATATAATTGGAAGATCATCAAAATGTGGTGAAAGTTTGGATATTTTTTTGAAAGCCTCTTGGTTGGCTAGAGGGTTTCAAGTTTTTTTTTTTTTTTTTGCAGCCGAAATGTAGAGAGAGGGAGAGATCTGAGTTGAGATTTCATATGGATACTG

CDS Sequence

Protein Sequence