Given a passage with a question and an answer to that question, classify if the answer actually answers the question into 'yes' or 'no'. Output 'yes' if the answer answers the question and output 'no' if the answer does not answer the question.

Q: Question: Do gene expression and genetic analysis reveal diverse causes of recessive self-compatibility in Brassica napus L?
Answer: The recessive SC in eight accessions is caused by the loss of function of BnSCR-7 and BnSCR-6 in pollen. Translational repression contributes to the recessive SC in three accessions, whose SRK and SCR genes were expressed normally and had identical CDSs to BrS-29 or BoS-15. SI in 11 F1 hybrids relies on the expression of BnSCR-1300 rather than SRK genes. Other factor(s) independent of the S locus are involved in recessive SC. Therefore, diverse causes underlie recessive SC in B. napus, yielding insight into these complex mechanisms.

A: yes
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Q: Question: Is expression of epigenetic modifiers significantly altered by exposure to secondhand smoke?
Answer: Quantification of the expression of genes encoding DNA methyltransferases (Dnmt1, Dnmt3a, Dnmt3b and Dnmt3l), methyl binding domain proteins (Mecp2, Mbd2 and Mbd3) and histone deacetylases (Hdac1 and Hdac2) by quantitative reverse-transcription polymerase chain reaction analysis showed modest but not statistically significant differences in the relative transcription of these key epigenetic regulators between SHS-exposed mice and age-matched controls. The non-significant changes in the expression of main epigenetic modifiers in SHS-exposed mice imply that SHS may predominantly induce genotoxic effects, particularly at non-tumorigenic doses, whereas epigenetic effects may only be secondary and manifest en route to tumor formation.

A: no
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Q: Question: Does 5 ' flanking region polymorphism of the gene encoding leukotriene C4 synthase correlate with the aspirin-intolerant asthma phenotype in the United States?
Answer: Our data demonstrate that the C-444 allele in the LTC4S gene is not statistically different among patients with the aspirin-intolerant asthmatic phenotype, patients with the aspirin-tolerant asthmatic phenotype, and unaffected control subjects in the United States. This finding, along with the lack of functionality of this polymorphism, suggest that it is not related to a specific asthma phenotype and may represent a population-stratified polymorphism within patients of eastern European descent.

A:
no
****