(Alliance, FBgn0003889 )

Tubulin is the major constituent of microtubules. It binds two moles of GTP, one at an exchangeable site on the beta chain and one at a non-exchangeable site on the alpha chain.

(UniProt, P61857)

A structural gene for β-tubulin. It is transcribed into mRNA that is testis-specific; the mRNA is translated into a β-tubulin subunit that is involved in the formation of microtubules in the sperm tail axoneme, the cytoplasmic microtubules, and the meiotic spindle (Kemphues et al., 1982; Fuller et al., 1988). Only the microtubules of the mitotic spindle are not affected by a null mutation in βTub85D. The first mutant discovered, βTub85DD (Kemphues et al., 1979, 1980, 1982, 1983), codes in males for an electrophoretic variant of β2-tubulin that causes disruption of microtubule function in all stages of spermatogenesis (beginning with meiosis) and shows abnormal spindle formation, abnormal chromosome movement, and no cytokinesis. This phenotype is expressed in males in both homo- and heterozygotes; mutants heterozygous over wild type contain both wild-type and mutant β2-tubulins; mutants over a deficiency for the locus contain only mutant β2-tubulin. Severity of effect on meiosis is as follows: βTub85DD/βTub85DD > βTub85DD/+ > βTub85DD/+/+, the first two genotypes being sterile and the last weakly fertile. All females are fertile. Chromosome replication and condensation appear normal. Recessive male-sterile mutations have also been induced, two of them in βTub85DD chromosomes and the rest in βTub85D+ chromosomes. Testes of flies homozygous for the recessives βTub85D3, βTub85D4, βTub85DDrv1, and βTub85DDrv2 synthesize, but later degrade, both α-Tubulin and β-tubulin and show abnormalities in meiotic divisions, nuclear shaping, and formation of the flagellar axoneme (Kemphues et al., 1982, 1983; Fuller, 1986). The most extreme recessive allele, βTub85Dn, is male sterile but female fertile when homozygous (Fuller et al., 1988); heterozygotes raised at 25 are male fertile, but those raised at 18 are male sterile. Recessive alleles βTub85D6 - βTub85D10 seem to accumulate normal amounts of β-tubulin but the β-tubulin subunits are defective. βTub85D6, βTub85D7, and βTub85D8 cause different defects in spermatogenesis. βTub85D8 is unable to form normal closed microtubules (Fuller et al., 1987); in homozygous males it is defective in meiosis, nuclear shaping, and flagellar elongation. This allele is semi-dominant; heterozygous males with one normal and one abnormal tubulin subunit, form some functional sperm. Transheterozygotes between ms(3)nc (second site non-complementing) mutations and certain βTub85D alleles are male sterile even if wild-type copies of both genes are present (Fuller, 1986); a deletion of a ms(3)nc mutation in a heterozygote over βTub85Dn, however, is fertile in males.