FASCIATION AND HETEROSIS IN PEA

44 RESEARCH REPORTS

PNL Volume 12 1980

Lonnig, W. E.

Institute of Genetics, Bonn, Federal Republic of Germany

Under the climatic conditions of Central Europe, our fasciated mutant

489 C always causes a strong heterotic effect in stem length, seeds per plant,

and other characters when crossed with the initial line (IL) 'Dippes gelbe

Viktoria', other lines, or different mutants (Fig. 1). Mutants 251 A, 123,

and other fasciated forms genetically comparable with mutant 489 C cause a

similar, but in some cases clearly weaker, heterotic effect (2).

As perhaps more than 15 genes are mutated in

489 C, it is not possible to say prima facie whether

one or more of the genes causing fasciation or other

unrelated mutant genes contribute to the heterotic

effects. Nor is it clear whether the phenomenon

is caused by a) heterozygosity per se, b) dominant

factors "hidden" or impeded by detrimental recessive

genes in the same mutant [most of the 15 genes have

mutated to the recessive state, as, for instance,

the genes for fasciation, but a few of them are

dominant in relation to the IL, as lateness in

flowering and ripening, sensitivity to day length

(4), and, perhaps, the genes for increased stem

length], c) gene interactions, or d) a combination

of the above.

In seeking answers to these questions, we used

the following mutants and recombinants for our

studies (all forms are derived from Dippes gelbe

Viktoria): a) strongly fasciated mutants 489 C,

33 A, b) linearly fasciated mutant 251 A, c) linearly

fasciated recombinants R 859 (derived from 123 x

46 C), R 661 (derived from 489 C x 26), and R 667

(derived from 489 C x 169), d) weakly fasciated

recombinants, stem bifurcated, R 161 (derived from

489 C x 1201 A) and R 177 (derived from 489 C x

1202 A), e) other mutants 176 A—narrow leaves,

flowers, and pods, 1201 A—stem bifurcated, 1001 —

Fig. 1.

489C 1201A

489C

1201A

thousand-grain weight increased.

The results of these crosses are shown in Fig. 2

and can be summarized as follows: a) 33 A, R 161,

R 661, and R 859 do not cause heterosis; the small

deviations are well in the range of the IL. This

means that the genetic causes for strong, linear, and weak fasciation are

not necessarily correlated with the heterotic effects, b) R 177 x IL, etc.,

do not show heterosis in length although the character "seeds per plant" seems

to show significant heterosis. For final analysis the crosses should be

repeated with more extensive material. If verified, there would be no strict

correlation between heterosis in length and yield, c) linearly fasciated

R 667 seems to cause a strong heterotic effect, comparable to that of 489 C

x IL, etc. However, 667 x IL is not very representative as we had only nine

46 RESEARCH REPORTS

PNL Volume 12

1980

The following facts seem to support the working hypothesis for special

importance of the genes for increased stem length and, perhaps, lateness:

1) Where there was no detectable heterosis in length in the F1, no long plants

were found in F2; unusual length doesn't seem to be a simple hypostatic

factor. None of these F1's was late. 2) The height of the hybrids was, of

course, a function of internode number and—even more important in this case—

internode length. Keeble and Pellew (1910) found both characters to show

dominant inheritance in crosses between non-fasciated lines. The situation

is, however, sometimes very complex. 3) The fasciated mutants causing hetero-

sis show an increase, especially in the number of internodes (Milutinovic,

1972), but the total length of internodes may be counteracted by recessive

genes. Fasciation itself may affect the length. Since the uppermost inter-

nodes of strongly fasciated mutants are extremely shortened, one could imagine

that the length of these internodes is longer in the F1 as a result of the

action of alleles for normal stem growth contributed by the IL. Strongly

fasciated mutants which do not cause heterosis are usually smaller than the

IL and, as mentioned above, may not possess the genes for special length and

lateness. Most of the linearly fasciated mutants induce weaker heterosis

in many characters. 4) Many of the recombinants derived from crosses of 489

C x IL (and different mutants) show increased length and yield (3, 4). Most

of them are late.

Further research will prove, modify, or disprove some of the above-

mentioned points in relation to heterosis. Other determinants (heterozygosity

and/or gene interactions) may be involved in an entirely satisfying explanation

of this case of heterosis.

1. Bandel, G. and W. Gottschalk. 1978. Z. Pflanzenzuchtg. 81:60-76.

2. Gottschalk, W. 1977. J. Nuclear Agric. Biol. 6:27-33.

3. Gottschalk, W. and G. Bandel. 1978. Z. Pflanzenzuchtg. 80:117-128.

4. Hussein, H. A. S. 1978. PNL 10:23.



	PNL Volume 12 1980	RESEARCH REPORTS 45

	plants in F1. According to the results, under a) the genetic cause for fas- ciation may not be the direct cause of this heterosis either. Segregation: Wherever a marked heterosis effect was evident in F1, all the segregations studied so far in F2 showed a majority (sometimes more than three- quarters) of plants as long as the F1 hybrids. However, a simple 3:1 segre- gation is excluded by several hypostatic genes segregating for shorter plants of different length.


	Fig. 2. F1's of the crosses