Part II of this series gives a classification, based on blackarm resistance, of over 160 varieties and strains of cotton. Complete immunity was not found in any New World types but exists in some of the Old World species. Several of the results disagreed with statements by St Vincent workers, some of the strains classed as “somewhat resistant”, “highly resistant” and “immune” by them being found at Shambat to be fully susceptible. It is suggested that St Vincent results were based on differences in primary infection (seed infection), rather than on true tissue resistance and that these differences were accentuated by the presence or absence of seed fuzz and by plant vigour.

Part III shows the type of blackarm resistance inheritance obtaining in the crosses Uganda B. 31 × 514 and B. 31 × 513 (all three are American Upland types) the latter results being further clarified by crosses between 513 and Sakel.

Uganda B. 31 contains resistance factorsB₁ andB₂ plus modifiers and shows grade “3” resistance; 514 contains no major resistance factors but numerous minor ones and is graded as “10” (grade “0” represents immunity and “12” full susceptibility). The first backcross to 514 gives a bimodal curve with peaks at grades “4” and “9” and displaying an approximate 1 : 1 ratio instead of the 3 : 1 ratio expected. InF₂ and in theF₂ of this first backcross, bimodal curves are again obtained, but these bear some resemblance to the 12 : 3 : 1 ratio expected. The reasons for these anomalies are discussed.

It is shown that 513, a selection from a Punjab American Upland importation with grade “5”–“6” resistance, contains factorB₂ together with several very weak resistance factors.

In theF₂ of a cross between two American Upland (G. hirsutum) types, Uganda B31 and the Sudan variety 514, a number of markedly dwarfed, ‘bunched-up’ plants appeared. Investigation showed that normality as opposed to ‘Dwarf-bunched’ depends on the presence of either of two duplicate genes, one dominant and the other giving an intermediate heterozygote. These genes have been calledD_a andD_b, the former deriving from 514 and the latter from Uganda B31. 514 is ofD_aD_ad_bd_b genotype, Uganda B31 isd_ad_aD_bD_b, Dwarf-bunched isd_ad_ad_bd_b, and the heterozygoted_ad_aD_bd_b shows considerable variability with a range from dwarf to normal.

The gened_b occurs in Gambia Native (G. hirsutum var.punctatum) and in the American Upland varieties Uganda SP84, XA129 and Deltapine, but it was not present in all Upland varieties examined.

The gened_a is closely linked with (or possibly identical with) the blackarm-resistance geneB₁. SinceG. barbadense types are ofD_aD_aD_bD_b composition,B₁ can be utilized in conferring blackarm resistance on this group. Its use within, theG. hirsutum group is fraught with the danger of producing, Dwarf-bunched types as the end-product.

A strong, partially dominant gene governing resistance to blackarm disease (Bact. malvacearum) has been transferred fromGossypium arboreum toG. barbadense (Domains Sakel). The new gene,B₄, segregates independently ofB₁,B₂, andB₃ and it shows additive effect in conjunction withB₂ and withB₃.

Three cytogenetically distinct techniques for transferring genes from Old World diploid to New World allopolyploid cottons are described and their relative merits discussed.

The immunity of Multani cotton (a variety ofGossypium arboreum racebengalense) toBact. malvacearum is shown to depend on a major gene,B₄, accompanied by a strong complex of minor genes. No such strong complex has ever been found in cottons of immediate New World origin. From this and other data, it is argued that the cottons of India have undergone a strong selection pressure fromBact. malvacearum for longer than the cottons of the New World, and it is suggested that this disease originated in the Old World—probably in India.

Two forms of resistance occur inGossypium barbadense: weak resistance, due to leaf hardening, is found in the Sea Islands, and strong resistance, due to the geneB₅ fortified by minor genes, occurs in the perennial variety Grenadines White Pollen.B₅ is variable in expression but, in general, the homozygotes show stronger resistance than the heterozygotes.B₅ is additive in conjunction withB₁, B₂, B₃ andB₄ respectively.

The character Withering Bracteole inGossypium hirsutum is shown to be controlled by a single recessive genebw. This gene has a pleiotropic action causing leaf crumpling and also sterility to a greater or less extent. Pollen grains carryingbw appear to have an advantage in fertilization.

At a low modifier levelF₂ ratios of 2·1 Normal: 1 Withering Bract were obtained, andbwbw plants were more or less sterile and had severely crumpled foliage. At a higher modifier levelF₂ ratios rose to 7·2∶1, presumably because many of thebwbw plants were indistinguishable from normal. In such families the deleterious effects ofbw were largely masked, but as a result the bracteoles also failed to wither effectively. This gene is therefore considered to be useless as a means of removing the bracteoles to facilitate mechanical picking.

It has been proved by workers elsewhere that hairs of sufficient length and density, on the undersides of cotton leaves, confer immunity to jassid. The resistance of Carpulla and Tanguis, twoGossypium barbadense perennial types, is shown to be due to a basic, partially dominant, hairiness gene designated,H₁, accompanied by a number of minor hairiness genes.H₁ is identical with the gene previously calledH^B andH^tan by Harland.

The jassid resistance of MU 8b, aG. hirsutum commerical type from India, is controlled byH₁ accompanied by intensifying genes which augment the effect ofH₁.H₁ also provides the genetic basis for the resistance found in St Ignatins, a variety ofG. hirsutum var.mariegalante from British Guiana.

Resistance in Kapas Purao was found to depend on a gene phenotypically similar toH₁ accompanied by hair length intensifiers. It appears to be linked to, or possibly identical with, one of two complementary genes controlling chlorosis.

A hair density gene,H₂ (identical with Harland’s,H^TO), is responsible for the dense tomentum ofG. tomentosum.

A blackarm resistance-intensifying gene, B_6m, has been transferred from Gossypium arboreum to Sakel (G. barbadense). By itself, B_6m confers no resistance, but in G. arboreum it is associated with, the gene B₄.

The G. hirsutum resistance gene, B_2, is stronger than B₄ when both are transferred to Sakel background. For this reason the new gene B_6m is being transferred to commercial synthetic blackarm-resistant Sudan Sakel and Upland (hirsutum) types carrying B₂ and B₃. In these combinations B_6m confers in the Sudan a resistance closely approaching immunity, and this resistance appears to be retained under Uganda conditions.

The blackarm resistance of the Upland variety Stoneville 20 is due to a major dominant gene,B₇, fortified by minor genes. This gene has been transferred to Sudan Sakel, on which background it is weaker in expression than the standard Upland resistance geneB₂.

The gene controlling hairiness in the Upland variety Pubescent T611 has been transferred to Sakel and shown to be identical with theG. tomentosum geneH₂.

Two Upland (Gossypium hirsutum) varieties (Kapas Purao and Philippines Ferguson) and apunctatum cotton of unknown origin, were all shown to carry a key hairiness gene at theH₁ locus. This gene is so closely linked withchl₁ (one of the two complementary genes governing chlorophyll deficiency) that transferences of it to Sakel, which carrieschl₂, cannot produce strains homozygous for hairiness. This allele has been calledH₁^k, and it is considered probable that theH₁^k-chl₁ segment of chromosome is invertedvis-à-vis theH₁-Chl₁ segment in Sakel and in_{G. barbadense} in general, andvis-à-vis theH₁-chl₁ segment in MU8b and other_{G. hirsutum} varieties.

In addition toH₁^k, Ferguson carries modifying genes which lengthen the hairs, minor H genes which can themselves directly confer hairiness, and modifying genes reducing the density of hair population.

A major hairiness gene was transferred fromGossypium herbaceum (Wagad 8) to Sakel (G. barbadense) and shown to be identical withH₁, the usual key gene in hairiness control in New World cottons. Since theH₁ andchl₁ loci are linked in New World cottons it follows that both belong to theA genom. In addition toH₁, Wagad 8 carries minorH genes and modifying genes affecting hair length.

Resistance to blaokarm disease (Xanthomonas malvacearum) inGossypium anomalum (n = 13;B genom) is controlled by a single recessive gene,b₈. This gene has been transferred toG. arboreum where it confers resistance rather less than that typical ofG. anomalum. The extra resistance ofG. anomalum is presumed to be due to factors for rapid leaf hardening evolved in response to the requirements of the xerophytic environment of this species. The geneb₈ is closely linked withR₂^os inG. anomalum.

A major hairiness gene was transferred from tetraploidGossypium arboreum (Multani) to Sakel and shown to be allelic to and closely similar toH₁. The geneH₁ is the key factor in hairiness control in the cultivated New World Cottons.

The resistance of Baumforth A toAmphorophora rubi (Kalt.), is shown to be controlled by a single dominant gene,A₁, which is linked with the normal allele of a semi-lethal gene,fr, designated Frilly. The cross-over value of these two loci is approximately 3·3%. The geneA₁ confers high resistance both to the seedling and to the mature plant.

Two partially dominant genes governing resistance to blackarm (Xanthomonas malvacearum) have been transferred fromGossypium herbaceum (n=13,A₁ genome) to Sakel,G. barbadense (n=26, (AD)₂ genome). The stronger of these genes has been given the symbolB₉; no symbol has been allocated to the weaker gene because gene homology tests have not been made between this and the other known genes.