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SEMAPHORE1 functions during the regulation of ancestrally duplicated knox genes and polar auxin transport in maize

Botany Department, University of Georgia, Athens, GA 30602, USA

View larger version (41K): [in a new window]   Fig. 1. Kernel phenotypes of semaphore1 mutants. (A) Portion of a self-pollinated ear from a sem1-R/Sem1 heterozygous plant, segregating for approximately one in four mutant kernels (arrow). (B) Mutant kernels (lower tier) contain both a smaller embryo (em) and endosperm (en) than non-mutant sibling kernels (upper tier). (C) Non-discordant kernels are generated following pollination of sem1-R/Sem1 heterozygous plants by plants harboring the B/A translocation TB-9Sd. The kernel on the left contains a hypoploid, mutant endosperm (genotype sem1-R/sem1-R/–) and a purple, hyperploid non-mutant embryo (genotype sem1-R/Sem1/Sem1). The sibling kernel on the right contains a hyperploid, purple non-mutant endosperm (genotype sem1-R/sem1-R/Sem1/Sem1) and a hypoploid, mutant embryo (genotype sem1-R–).

View larger version (142K): [in a new window]   Fig. 2. Ectopic KNOX accumulation in semaphore1 mutant seedlings. Immunohistolocalization of vegetative shoots using a polyclonal KNOX antibody. (A,D) non-mutant siblings, (B,E) moderate sem1 mutant seedling, (C,F) severe mutant seedling. The arrows in D and E indicate the position of the incipient leaf primordium (labeled 0); the two youngest leaf primordia in E are numbered. The arrow in F indicates the expected position of the shoot apex. Scale bars: 200 µm, in A for A-C and in D for D-F.

View larger version (119K): [in a new window]   Fig. 3. Embryo development is abnormal in semaphore mutants. KNOX immunohistolocalizations of 12 DAP embryos. Non-mutant embryos (A,B) are larger than sem1 mutant siblings (C-H) and show no KNOX accumulation in the incipient leaf (arrow in B and D), leaf primordia (numbered), pericarp (p), scutellum (s), coleoptile (c) or endosperm (en). Moderately retarded sem1 mutants (C-D) and more severely retarded mutants (E-H) exhibit ectopic KNOX accumulation in the endosperm and fewer (if any) leaf primordia than non-mutant siblings. The arrows in F and H indicate the shoot meristem. Scale bars: 200 µm, in A for A,C,E,G and in B for B,D,F,H.

View larger version (70K): [in a new window]   Fig. 4. Mutant leaves show ectopic expression of rough sheath1 and gnarley1 transcripts. Following 40 cycles of RT-PCR, rs1 (A) and gn1 (B) transcripts are detected in sem mutant adult leaves. Inconsistent results are obtained using lg3-specific primers (B). (C) Semi-quantitative RT-PCR of kn1, gn1 and kn1 transcripts in sem1-R mutant (top), rs2-R mutant (center) and non-mutant B73 seedling leaves (bottom). No knox transcripts are detected in non-mutant leaves (Fig. 4A, B, C bottom), even after 50 RT-PCR cycles (data not shown). Sizes of predicted RT-PCR products are: ubiquitin, 208 bp; rough sheath1, 625 bp; knotted 1, 342 bp; liguless3, 248 bp; gnarley, 190 bp, indicated by arrows to distinguish from primer-dimers.

View larger version (96K): [in a new window]   Fig. 5. Pleiotropic shoot phenotypes of sem1 mutants. (A) Adult sem1 mutant plants (right) have much shorter stems than non-mutant siblings (left). (B) The leaf blade (b), midrib (m), ligule (lg), auricle (au) and sheath of the non-mutant sibling leaf (left) are indicated. The black arrows in the mutant leaf (right) indicate the displaced and ectopic ligules. (C) Close up of the displaced ligule (lg) and two ectopic ligules (arrows) of a sem1 mutant leaf. (D) Ectopic sheath extensions (arrows) at the margins of the blade-sheath boundary in a sem1 mutant leaf. (E) Ectopic auricle formation (arrow) at the margin of a sem1 mutant leaf blade.

View larger version (161K): [in a new window]   Fig. 6. Disruptions of the blade-sheath boundary in sem1 mutant leaves. Scanning electron micrograph images of the epidermal surfaces of non-mutant (A), and mutant (B) leaf primordia soon after initiation of the ligule (arrows), separating the blade (b) from the sheath (s). The mutant ligule (B) is displaced distally in the midrib region. (C) Non-mutant young adult leaf at maturity. lg, ligule. (D) The non-mutant midrib and blade (b) distal to the ligule depicted in C. (E-I) Images of a sem1 mutant, young adult leaf showing ligule displacement over the midrib (E), an ectopic second ligule (F), the region distal to the ectopic second ligule (G), an ectopic third ligule (H), and (I) normal cell types located distal to the disturbed region. Scale bar: 300 µm.

View larger version (61K): [in a new window]   Fig. 7. Abnormal vasculature in sem1 mutant leaves. (A) Ectopic proliferation of margin tissue at the blade-sheath boundary of a mutant leaf shows extensive transverse vasculature elements. b, blade; s, sheath; l, ligule. (B-G) Cleared and stained sheath tissue of (B-D) non-mutant and (E-G) sem1 mutant leaves. (B,E) Just proximal to the ligule and midway between the midrib and margin. (C,F) As in B and E, but 4 cm proximal to the ligule. (D,G) Near the margin, 4 cm proximal to the ligule. The sem1 mutant sheath shows poor development of transverse veins. Scale bar in B: 50 µm for B-G.

View larger version (76K): [in a new window]   Fig. 8. (A) Adult sem1 mutant leaf showing yellow, zebra striping. (B,C) Impaired root development in sem1 mutants. (B) Root development in a non-mutant seedling. Arrow, hypocotyl (seedling stem). (C) Root development in a sem1 mutant seedling. (D,E) Transverse sections of the hypocotyl in non-mutant siblings (D) and in smaller mutant plants (E) reveal no gross abnormalities in vascular development in sem1-R mutant seedlings. Scale bar for D and E, 50 µm.

View larger version (15K): [in a new window]   Fig. 9. Basipetal auxin transport is impaired in hypocotyls of sem1 mutant shoots. Each value represents the mean of 5 individual hypocotyl segments, as described in Materials and Methods.