University of Milan
Shoot meristemless (sml) mutant in maize
--Pilu, R, Mencarelli, M, Tamagnone, L, Consonni, G, Gavazzi, G

The shoot meristemless (sml) phenotype was selected as a putative non germinating mutant in a line obtained by selfing F1 plants heterozygous for Ac and r-scm3. This mutant (originally named emb 7190 as previously reported in MNL 72:58 ), shows up at germination, since primary root protrusion is not associated with shoot emergence. Other shootless mutants (ed-41v and dks8) in our collection, that have been studied by Dr. C. Rivin, are not allelic to sml.

Longitudinal sections of immature (16 DAP) sml mutant embryos show a normal root primordium while a shoot meristem is not recognizable. In its place several meristematic-like cells are found intermingled with nonmeristematic ones, suggesting that the mutant is unable to recruit meristematic cells into the orderly structure of a SAM (Figure 1).

In its original background (W22) the mutant segregates 3:1. If heterozygous plants are outcrossed to A344 or A188 inbred lines and the F1 is selfed, the F2 consists of normal (wt), distorted growth (dgr) and shoot meristemless (sml) seedlings in a 12:3:1 ratio.

Seedlings with distorted growth are characterized by abnormal growth of the coleoptile and internodes and, in some cases, by the appearance of two or more shoot apexes or of a root replacing the shoot. During development leaves do not expand and plants do not elongate. Mature plants exhibit a bushy growth habit (Figure 2).

The data reported in Table 1 are best interpreted by assuming that the sml phenotype results from the interactions of two recessive factors: sml and dgr (distorted growth). The distorted growth phenotype (Figure 2) is attributable to a partial recovery of the sml phenotype, possibly exerted by the Dgr allele on the sml/sml genotype. Presence of one functional dose of Dgr allows bypass of the meristematic block induced by sml by promoting some shoot morphogenesis even though without allowing total recovery. The statistical analysis (c2 test) performed on the data shown in Table 1 confirms the hypothesis of a recessive epistatic interaction.

The sml gene has been mapped on chromosome 10L and experiments to delimit its location more accurately are in progress.

Table1. Results of F2 segregations obtained in selfed progeny of the mutant outcrossed to different inbred lines.
Inbred wt dgr Sml
A188 430 - 136
A344 108 40 10
B73 282 64 20

Figure 1. Longitudinal sections of wt and sml embryos at 16 DAP stained with toluidine blue. Note the presence of putative meristematic cells in the area where the shoot apical meristem (SAM) should be. It seems as if these meristematic cells are not recruited into the orderly structure of the SAM with its characteristic zonation. a) coleoptile, b) first leaf, c) shoot apical meristem, d) second leaf bulge, e) root meristem, f) meristematic-like cells.

Figure 2. Distorted growth (DGR) phenotype at maturity.

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