A gametophyte factor on chromosome 9 affects both male and female gametophytes --Fowler, JE My lab recently became interested in mutations that affect the maize male gametophyte. A search of MaizeDB revealed several ga* (gametophyte factor) "phenotype only" stocks, which have not been extensively characterized. We obtained these stocks from the Maize Genetics Cooperation Stock Center (Co-op) and are investigating their effects on pollen development.

I confirmed that one of these factors, designated ga*-94-764, maps to chromosome 9, near bz1 sh1. Exact reciprocal crosses with a homozygous tester showed that the ga allele caused a transmission defect through both male and female gametophytes that is significantly different from the expected 1:1 ratio (Table 1). No recombinants in the bz1-sh1 interval were obtained, so the location of the ga factor with respect to these loci is unknown.

Table 1. Reduced transmission of ga-linked markers through male and female gametophytes. Each cross shows the results of a ga* + +/ + sh1 bz1 heterozygote crossed to a sh1-bz1-m4 homozygote.
 
 
ga through male
 
ga through female
 
Cross
bz sh (%)
Bz Sh (%)
Chi-Square
bz sh (%)
Bz Sh (%)
Chi-Square
1
210 (74)
72 (26)
67.5
136 (69)
60 (31)
29.5
2
288 (77)
85 (23)
110
52 (81)
12 (19)
25
3
192 (78)
54 (22)
77.4
36 (71)
15 (29)
8.6

The stock from which these data were derived is marked "from lo2 stock". Given that lo2 causes abortion of the female gametophyte, and that it also maps in the vicinity of bz1 sh1, ga*-94-764 could be a derivative of the original lo2 allele. Alternatively, it could be a new allele of the ga8 locus, which also maps to 9S, but is not available from the Co-op; or, this allele could define a novel locus. Until further mapping data allow us to distinguish among these possibilities, I suggest that this allele be referred to as ga*11.

Ears in which the ga* allele was transmitted through the female gametophyte were unfilled (Figure 1A), suggesting that the allele caused a defect in the female gametophyte, in fertilization, or very early in embryonic development.

In addition, transmission of the ga-linked Sh1 Bz1 alleles through the male was reduced at the bottom of the ear, relative to the top (Figure 1B, Table 2). These results indicated that ga* pollen was at a competitive disadvantage in longer silks, i.e., those leading to the egg sacs at the bottom of the ear. Thus, the ga* pollen may grow at a slower rate than wild-type pollen. Two other ga loci (ga7 and ga10) did not exhibit such a top-to-bottom gradient within the ear (data not shown). Thus, mutations that cause reduced transmission through the male can be separated into two distinct phenotypic classes, based on the distribution of linked kernel markers on the ear.

In similar experiments using two other ga* stocks from the Co-op (ga*-Rhoades, linked to bt1; and ga*-0188, linked to pr1), I was not able to confirm that either of the ga* alleles adversely affected transmission through male or female gametophytes.

Figure 1. Ears from Cross 2, in Table 1. The top of each ear is to the left. A) The ga* heterozygote was the female parent. B) The ga* heterozygote was the male parent.

Table 2. Spatial distribution (top-to-bottom) of kernels of a given phenotype on ears that were derived using the ga* heterozygote as the male parent. Ears were divided in thirds, based on length. Chi-Square tests rejected the hypothesis that distribution of kernels of a given phenotype is unaffected by their position along the length of the ear (df=2, P value <0.001 for two ears, <0.05 for one ear).
 
   
bz sh 
(%)
Bz Sh
(%)
Chi-Square
Cross 1              
  Top
62
(64)
35
(36)
   
  Middle
68
(72)
26
(28)
   
  Bottom
80
(88)
11
(12)
   
           
14.6
<0.001
Cross 2              
  Top
74
(63)
43
(37)
   
  Middle
96
(78)
27
(22)
   
  Bottom
118
(89)
15
(11)
   
           
23.0
<0.001
Cross 3              
  Top
69
(77)
21
(23)
   
  Middle
52
(70)
22
(30)
   
  Bottom
71
(87)
11
(13)
   
           
6.20
<0.05

 
 
 


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