Abstract
The regulation of antagonistic OVO isoforms is critical for germline formation and differentiation in Drosophila. However, little is known about genes related to ovary development. In this study, we cloned the Bombyx mori ovo gene and investigated its four alternatively spliced isoforms. BmOVO-1, BmOVO-2 and BmOVO-3 all had four C2H2 type zinc fingers, but differed at the N-terminal ends, while BmOVO-4 had a single zinc finger. Bmovo-1, Bmovo-2 and Bmovo-4 showed the highest levels of mRNA in ovaries, while Bmovo-3 was primarily expressed in testes. The mRNA expression pattern suggested that Bmovo expression was related to ovary development. RNAi and transgenic techniques were used to analyze the biological function of Bmovo. The results showed that when the Bmovo gene was downregulated, oviposition number decreased. Upregulation of Bmovo-1 in the gonads of transgenic silkworms increased oviposition number and elevated the trehalose contents of hemolymph and ovaries. We concluded that Bmovo-1 was involved in protein synthesis, contributing to the development of ovaries and oviposition number in silkworms.
Highlights
In Drosophila, isoforms of OVO-B and OVO-A are produced by two major classes of germline ovo transcripts driven by the ovoA and ovo-B promoters [1,2]
Three Polymerase chain reaction (PCR) products of 2.4, 0.8 and 0.5 kb were amplified from testes and ovary cDNA
Silkworm ovaries have different Bmovo transcripts and isoforms In B. mori, the ovo gene region produces at least 4 transcripts and is different from the D. melanogaster shavenbaby-ovo gene region
Summary
In Drosophila, isoforms of OVO-B and OVO-A are produced by two major classes of germline ovo transcripts driven by the ovoA and ovo-B promoters [1,2]. Ovo-B and ovo-A transcripts differ only in their short first exons; OVO-B has 374 fewer residues than OVO-A. Ovo-B mRNA encodes the OVO-B isoform from an AUG initiation codon in exon 2, and the ovo-A transcript encodes the longer OVO-A isoform. OVO-B and OVO-A are transcription factors with opposing regulatory activities that are required for female germline survival and oogenesis [4]. All four ovoD mutations introduce novel in-frame AUG codons upstream of the ovo-B initiation codon that the result in ovo-B transcripts that encode slightly truncated ovo-A isoforms. OVO-B expression is high during oogenesis, but OVO-A is expressed very weakly and only in nearly mature follicles [2,4]
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