Background

Pigs that carry two copies of the halothane gene, also known as the PSS (porcine stress syndrome) gene, have long been known to exhibit extreme sensitivity to stress, including sudden death when stressed, and produce pale soft watery meat (known as PSE meat - pale, soft, exudative). The same gene also causes increased leanness and feed efficiency. Pigs carrying one copy of the gene (known as heterozygotes) are not susceptible to stress, but it is believed that they show some increase in leanness. It is uncertain whether, and if so to what degree, these heterozygotes also produce PSE meat. On the belief that heterozygotes show increased leanness but not PSE, it has been suggested that heterozygotes might have an economic advantage over normal homozygotes that carry no copies of the PSS gene.

Close to the beginning of the OPCAP, a DNA test came available which for the first time allowed heterozygotes to be identified. Applying this test to OPCAP pigs provided the opportunity to accurately assess the growth and carcass characteristics of heterozygotes on a scale and level of detail not previously possible.

Methods

The HAL-1843^TM test was used to determine the PSS genotype of some 2900 pigs in the project based on DNA extracted from lean meat, fat and blood samples. Methods of statistical analysis of data are described in Appendix 3. All estimates presented here are from reduced models with all non-significant effects removed. In the following description of results, differences between heterozygotes and homozygotes are described as percentages of the homozygote performance.

Results

The numbers of pigs of each genotype for each breed are shown in Table 1. There were only seven homozygote mutants in the whole project, and the frequency of heterozygotes was quite low, ranging from 6 to 15% across breeds. There was no statistical evidence of decline in frequency across the three years of the project, but it is known that many participants were using the test to eliminate the gene from their populations and we would expect much lower frequencies today.

Estimates of the effect of the gene on growth and carcass characteristics are shown in Table 2. Homozygotes for the mutation were removed from the analysis, so gene effects are estimated only for heterozygotes (carriers) versus homozygous normal pigs that do not carry the gene.

There were no significant effects on growth, backfat (live animal and carcass), estimated lean yield, which is largely a function of backfat, or carcass index. Heterozygotes had a barely significant 1% favourable decrease in feed conversion, and a significant 0.5% increase in dressing percentage.

Heterozygotes had a somewhat different shape to homozygotes, being 0.5% shorter and having about 0.8% more of the carcass as ham, as well as being 5 to 10% thinner skinned. Heterozygotes showed a striking 2.5% increase in loin eye area compared to homozygotes. Heterozygotes also had a 1 to 1.6% higher lean content in each primal individually and across all three primals. Primarily because of the increased relative size of the hams, heterozygotes showed a 1% increase in the proportion of total lean in the three primals that came from the ham, while the contributions of lean from shoulder and loin decreased accordingly. Although not statistically significant, changes in chemical fat and lean in belly and loin were consistent with changes in other measures of carcass leanness.

Heterozygotes had a 10% lower marbling score, 6 to 8% lower meat colour scores, and 4 to 9% lower structure scores than heterozygotes. Drip loss of the loin was about 5% higher in heterozygotes, which approached statistical significance. There was no indication that the effects of the gene differed between barrows, gilts or boars. Similarly, the effect of the gene appeared to be the same across breeds, except for drip loss of the loin and ham, and colour and structure scores of the ham. For drip loss, Landrace showed no differences between heterozygotes and homozygotes, while differences for other breeds were somewhat larger than the across breed differences shown in Table 2. For structure score of ham, Durocs and Landrace showed essentially no difference between heterozygotes and homozygotes, while the reduced colour of the ham of heterozygotes was obvious for Hampshires, but not for other breeds.

Implications

It appears that heterozygotes exhibit both improved carcass leanness and feed conversion along with reduced meat quality. The detrimental effect on meat quality may be worse for Hampshires and Yorkshires than for Durocs and Landrace. Taken at face value, the detrimental effects on quality would probably negate any positive economic advantages of the heterozygote for feed conversion and leanness for Hampshires and Yorkshires, while heterozygotes may have a net positive economic advantage in Durocs and Landrace. However, statistical strength of the estimated breed differences in the effect of the PSS gene are rather weak, causing some uncertainty in this interpretation. Given the difficulties and cost of maintaining a sire line homozygous for the PSS gene in order to produce a heterozygote commercial product, it seems that for most breeders, elimination of the gene would be appropriate.

Table 1. Numbers and frequencies of PSS genotypes across breeds.

	Duroc	Hampshire	Landrace	Yorkshire	Total
Homozygous normal	489	262	628	1180	2559
Heterozygotes	43	17	115	136	311
Homozygous PSS	1	0	2	4	7
Frequency of heterozygotes	0.081	0.061	0.154	0.103	0.108
Frequency of PSS allele	0.042	0.030	0.080	0.055	0.056

Table 2. Least square means for PSS genotypes.

Trait	Homozygote (normal)	Heterozygote	Significance Level (p)1
Weight on test (kg)	31.6	31.4	0.29
Weight at slaughter (kg)	106.5	106.2	0.39
Days to 100 kg (d)	160.4	160.0	0.56
Average daily gain (kg/d)	0.866	0.867	0.89
Backfat at 100 kg (mm)	13.6	13.4	0.11
Feed conversion	2.66	2.63	0.04
Hot carcass weight (kg)	84.1	84.5	0.23
Dressing %	78.8	79.2	0.01
Estimated yield (old) (%)	51.0	51.1	0.71
Estimated yield (new) (%)	60.5	60.5	0.73
Carcass index (old)	106.9	107.1	0.54
Carcass length (cm)	82.8	82.4	0.03
Moisture loss (%)	1.31	1.29	0.71
Skin thickness, shoulder (mm)	2.10	1.90	0.04
Skin thickness, back (mm)	2.65	2.66	0.82
Skin thickness, loin (mm)	3.20	3.15	0.53
Skin thickness, chop (mm)	3.20	3.10	0.7
Loin eye area (cm2)	42.0	43.0	0.001
Max. fat depth, shoulder (mm)	40.8	40.7	0.68
Min. backfat (mm)	20.7	20.7	0.88
Min. loin fat (mm)	26.2	26.1	0.75
Shoulder % of side	28.8	28.7	0.45
Loin % of side	26.2	26.1	0.28
Ham % of side	26.6	26.8	<0.001
Belly % of side	18.5	18.5	0.89
Lean content of shoulder (%)	47.2	47.8	<0.001
Lean content of loin (%)	51.0	51.6	0.02
Lean content of ham (%)	61.3	62.2	<0.001
Lean content of 3 primals (%)	53.0	53.8	<0.001
Shoulder lean (% of 3 primals)	31.7	31.5	0.15
Loin lean (% of 3 primals)	30.3	30.1	0.06
Ham lean (% of 3 primals)	38.0	38.4	<0.001
Chemical fat, loin (% of DM)	17.52	16.47	0.09
Chemical protein, loin (% of DM)	11.85	11.98	0.25
Chemical fat, belly (% of DM)	64.90	63.41	0.15
Chemical protein, belly (% of DM)	4.88	5.09	0.14
Belly ratio 12	0.910	0.920	0.17
Belly ratio 22	0.083	0.097	0.13
Belly ratio 32	0.299	0.311	0.34
Loin drip loss (%)	10.8	11.3	0.10
Ham drip loss (%)	10.6	10.5	0.72
Marbling score, loin	2.12	1.90	<0.001
Ag. Canada colour, loin	2.70	2.50	<0.001
Jap. colour, loin	3.44	3.23	<0.001
Ag. Canada structure, loin	2.65	2.41	<0.001
Ag. Canada colour, ham	3.27	3.08	<0.001
Ag. Canada structure, ham	2.67	2.57	0.054

¹ A p value of less than 0.05 would usually be taken as statistically significant.
² See Appendix 2 for definitions.